2f:I[703058,["/_next/static/immutable/chunks/3bhq_5eh1d760.js","/_next/static/immutable/chunks/1855-ogyi8eh4.js","/_next/static/immutable/chunks/2pfsjpn6k6zlg.js","/_next/static/immutable/chunks/26c7v3_3uwnwu.js","/_next/static/immutable/chunks/25a3ozcrvi1ff.js","/_next/static/immutable/chunks/2r4wx50nvjh_4.js","/_next/static/immutable/chunks/23fsw06hsi5b1.js","/_next/static/immutable/chunks/06_yt270h41rg.js","/_next/static/immutable/chunks/3ezsiz-7shkna.js","/_next/static/immutable/chunks/20x2y96ldu5wx.js","/_next/static/immutable/chunks/2lxntcm3pd1_h.js","/_next/static/immutable/chunks/00dgco8irq3jw.js","/_next/static/immutable/chunks/00nwe-kq0rboc.js","/_next/static/immutable/chunks/2051ffx3xzio9.js"],"PaperListPageClient"] 30:T455,Innate lymphoid cells (ILCs) are tissue-resident lymphocytes that regulate tissue homeostasis and immune responses. How ILCs modulate T cells, remains incompletely understood. To investigate the interaction between ILCs and T cells, we differentiated ILC2s and ILC3s from hematopoietic stem cells (HSCs). Both suppressed T-cell proliferation, enhanced cytokine production, and upregulated T-cell senescence-associated surface receptors (CD57, KLRG1, TIGIT, and TIM3). T cells exposed to ILCs also increased expression of senescence-related proteins, including p16, p21, p53, GATA4, and NF-κB. Mechanistically, ILCs produced interleukin-9 (IL-9), and IL-9 blockade prevented ILC-driven T-cell senescence. Conversely, addition of exogenous IL-9 to T cells recapitulated the effects of ILC coculture. Finally, in both human xenogeneic and murine allogeneic hematopoietic cell transplantation models, we observed ILC-mediated T-cell modulation in vivo, with evidence of T-cell senescence. In conclusion, HSC-derived ILCs from both humans and mice mitigate graft-versus-host disease by inducing T-cell senescence.31:T4db, Abstract Innate lymphoid cells (ILCs) are tissue-resident lymphocytes that regulate tissue homeostasis and immune responses. How ILCs modulate T cells, remains incompletely understood. To investigate the interaction between ILCs and T cells, we differentiated ILC2s and ILC3s from hematopoietic stem cells (HSCs). Both suppressed T-cell proliferation, enhanced cytokine production, and upregulated T-cell senescence–associated surface receptors (CD57, KLRG1, TIGIT, and TIM3). T cells exposed to ILCs also increased expression of senescence-related proteins, including p16, p21, p53, GATA4, and NF-κB. Mechanistically, ILCs produced interleukin-9 (IL-9), and IL-9 blockade prevented ILC-driven T-cell senescence. Conversely, addition of exogenous IL-9 to T cells recapitulated the effects of ILC coculture. Finally, in both human xenogeneic and murine allogeneic hematopoietic cell transplantation models, we observed ILC-mediated T-cell modulation in vivo, with evidence of T-cell senescence. In conclusion, HSC-derived ILCs from both humans and mice mitigate graft-versus-host disease by inducing T-cell senescence. 32:T7c1,The current approach to minimize transplant-associated complications, including graft-versus-host disease (GVHD) includes long-term pharmacological immune suppression frequently accompanied by unwanted side effects. Advances in targeted immunotherapies regulating alloantigen responses in the recipient continue to reduce the need for pan-immunosuppression. Here, in vivo targeting of the tumor necrosis factor superfamily receptor TNFRSF25 (also known as DR3) and the high-affinity interleukin-2 (IL-2) receptor with a TL1A-immunoglobulin (TL1A-Ig) fusion protein and low-dose IL-2, respectively, was used to pretreat recipient mice before allogeneic hematopoietic stem cell transplantation (aHSCT). Pretreatment induced regulatory T cell (Treg) expansion persisting 1 to 2 weeks after HSCT, leading to diminished GVHD and improved transplant outcomes. Expansion was accompanied by an increase in the frequency of stable and active Tregs, creating a suppressive tissue environment in the colon, liver, and eye. Importantly, pretreatment supported epithelial cell function/integrity, a diverse microbiome including reduction of pathologic bacteria outgrowth, and promotion of butyrate producing bacteria, while maintaining physiologic levels of obligate/facultative anaerobes. Notably, using a sphingosine 1-phosphate receptor agonist to sequester T cells in lymphoid tissues, it was found that the increased tissue Treg frequency included resident CD69+CD103+FoxP3+ hepatic Tregs. In contrast to infusion of donor Tregs, the strategy developed here resulted in the presence of immunosuppressive target tissue environments in the recipient before the receipt of donor allogeneic-reactive T cells and successful perseveration of graft-versus-leukemia responses. We posit strategies that circumvent the need of producing large numbers of ex vivo manipulated Tregs may be accomplished through in vivo recipient Treg expansion, providing translational approaches to improve aHSCT outcomes.33:T845, Abstract The current approach to minimize transplant-associated complications, including graft-versus-host disease (GVHD) includes long-term pharmacological immune suppression frequently accompanied by unwanted side effects. Advances in targeted immunotherapies regulating alloantigen responses in the recipient continue to reduce the need for pan-immunosuppression. Here, in vivo targeting of the tumor necrosis factor superfamily receptor TNFRSF25 (also known as DR3) and the high-affinity interleukin-2 (IL-2) receptor with a TL1A-immunoglobulin (TL1A-Ig) fusion protein and low-dose IL-2, respectively, was used to pretreat recipient mice before allogeneic hematopoietic stem cell transplantation (aHSCT). Pretreatment induced regulatory T cell (Treg) expansion persisting 1 to 2 weeks after HSCT, leading to diminished GVHD and improved transplant outcomes. Expansion was accompanied by an increase in the frequency of stable and active Tregs, creating a suppressive tissue environment in the colon, liver, and eye. Importantly, pretreatment supported epithelial cell function/integrity, a diverse microbiome including reduction of pathologic bacteria outgrowth, and promotion of butyrate producing bacteria, while maintaining physiologic levels of obligate/facultative anaerobes. Notably, using a sphingosine 1-phosphate receptor agonist to sequester T cells in lymphoid tissues, it was found that the increased tissue Treg frequency included resident CD69+CD103+FoxP3+ hepatic Tregs. In contrast to infusion of donor Tregs, the strategy developed here resulted in the presence of immunosuppressive target tissue environments in the recipient before the receipt of donor allogeneic-reactive T cells and successful perseveration of graft-versus-leukemia responses. We posit strategies that circumvent the need of producing large numbers of ex vivo manipulated Tregs may be accomplished through in vivo recipient Treg expansion, providing translational approaches to improve aHSCT outcomes. 34:T8f6,Vitiligo is a multifactorial, depigmenting skin disorder characterized by selective loss of melanocytes. Large-scale studies are lacking to determine the risk of vitiligo in transplant recipients with graft-vs-host disease (GVHD). To investigate the incidence rates and risk of vitiligo in patients who had received solid organ transplant (SOT) or hematopoietic stem cell transplant (HSCT) overall and by HSCT graft type and concomitant GVHD. This population-based cohort study included data from the National Health Insurance Service database of Korea for patients aged 20 years or older who had received a transplant (SOT or HSCT) between January 2010 and December 2017, with follow-up until December 2019. A cohort of age- and sex-matched (1:5) control individuals who did not receive a transplant was included for comparison. Data were analyzed from July 2021 to December 2021. Transplant (SOT or HSCT) and GVHD. The main outcome was risk of vitiligo, assessed using multivariable Cox proportional hazards regression analyses adjusting for potential confounding factors. The study included 23 829 patients who had undergone SOT or HSCT (62.78% male; mean [SD] age, 49.58 [11.59] years) and 119 145 age- and sex-matched controls. Patients who had undergone transplant had a significantly higher risk of vitiligo compared with controls (adjusted hazard ratio [AHR], 1.73; 95% CI, 1.35-2.22). Risk of vitiligo was also slightly higher in kidney transplant recipients and liver transplant recipients compared with the controls but was highest in HSCT recipients (AHR, 12.69; 95% CI, 5.11-31.50). Patients who had received allogeneic grafts (AHR, 14.43; 95% CI, 5.61-37.15), those who had received autologous grafts (AHR, 5.71; 95% CI, 1.20-3.18), those with comorbid GVHD (AHR, 24.09; 95% CI, 9.16-63.35), and those without GVHD (AHR, 8.21; 95% CI, 3.08-21.87) had a higher risk of vitiligo compared with controls. In this study, risk of vitiligo was significantly higher in transplant recipients, especially in HSCT recipients and those with allogeneic grafts or comorbid GVHD. These findings provide new insights into the association between the risk of vitiligo and transplant and GVHD. Clinicians should be aware of these risks, implementing a multidisciplinary approach for monitoring.35:Tbab,ImportanceVitiligo is a multifactorial, depigmenting skin disorder characterized by selective loss of melanocytes. Large-scale studies are lacking to determine the risk of vitiligo in transplant recipients with graft-vs-host disease (GVHD).ObjectiveTo investigate the incidence rates and risk of vitiligo in patients who had received solid organ transplant (SOT) or hematopoietic stem cell transplant (HSCT) overall and by HSCT graft type and concomitant GVHD.Design, Setting, and ParticipantsThis population-based cohort study included data from the National Health Insurance Service database of Korea for patients aged 20 years or older who had received a transplant (SOT or HSCT) between January 2010 and December 2017, with follow-up until December 2019. A cohort of age- and sex-matched (1:5) control individuals who did not receive a transplant was included for comparison. Data were analyzed from July 2021 to December 2021.ExposureTransplant (SOT or HSCT) and GVHD.Main Outcomes and MeasuresThe main outcome was risk of vitiligo, assessed using multivariable Cox proportional hazards regression analyses adjusting for potential confounding factors.ResultsThe study included 23 829 patients who had undergone SOT or HSCT (62.78% male; mean [SD] age, 49.58 [11.59] years) and 119 145 age- and sex-matched controls. Patients who had undergone transplant had a significantly higher risk of vitiligo compared with controls (adjusted hazard ratio [AHR], 1.73; 95% CI, 1.35-2.22). Risk of vitiligo was also slightly higher in kidney transplant recipients and liver transplant recipients compared with the controls but was highest in HSCT recipients (AHR, 12.69; 95% CI, 5.11-31.50). Patients who had received allogeneic grafts (AHR, 14.43; 95% CI, 5.61-37.15), those who had received autologous grafts (AHR, 5.71; 95% CI, 1.20-3.18), those with comorbid GVHD (AHR, 24.09; 95% CI, 9.16-63.35), and those without GVHD (AHR, 8.21; 95% CI, 3.08-21.87) had a higher risk of vitiligo compared with controls.Conclusion and RelevanceIn this study, risk of vitiligo was significantly higher in transplant recipients, especially in HSCT recipients and those with allogeneic grafts or comorbid GVHD. These findings provide new insights into the association between the risk of vitiligo and transplant and GVHD. Clinicians should be aware of these risks, implementing a multidisciplinary approach for monitoring.25:[[["$","script","0",{"type":"application/ld+json","dangerouslySetInnerHTML":{"__html":"{\"@context\":\"https://schema.org\",\"@type\":\"CollectionPage\",\"name\":\"Graft-Versus-Host Disease: condition Research & Clinical Takeaways\",\"description\":\"Explore peer-reviewed papers on Graft-Versus-Host Disease (condition). Clinician-written summaries and actionable practice insights. 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Both VDP and VHI correlated with FEV1 (r=−0.74 and r=−0.73) and LCI (r=0.71 and r=0.72). Three of 6 non-BOS participants had abnormal FEV1 yet normal VDP and LCI, highlighting complementary information from Xe-MRI.","limitations":"- Very small sample (n=12 total, 6 per group) at a single center limits statistical power and generalizability.\n- Cross-sectional design prevents assessment of longitudinal tracking or early detection utility.\n- LCI data were missing in 2 BOS participants due to technical failure and participant inability, weakening MBW comparisons.","practice_takeaway":"In pediatric post-HSCT patients, Xe-MRI can reveal ventilation defects and heterogeneity not fully captured by FEV1 alone, which may help differentiate BOS from other causes of reduced FEV1. Clinicians should consider Xe-MRI and MBW as complementary, non-ionizing tools alongside spirometry for BOS surveillance in this population."}},{"doi":"10.1038/s41577-026-01345-8","pmid":"42686822","title":"Interleukin-33 and its receptor: multifaceted roles and emerging therapeutic potential","journal_title":"Nature Reviews Immunology","journal_issn":"1474-1733","published_at":"2026-09-02T00:00:00.000Z","url":"https://doi.org/10.1038/s41577-026-01345-8","source_score":16,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-06T06:23:00.811Z","updated_at":"2026-09-06T06:23:00.811Z","tags":[{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"category","value":"Immunology","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"condition","value":"Allergy","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"condition","value":"Asthma","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"condition","value":"Autoimmunity","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"condition","value":"Cancer","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"condition","value":"Chronic Obstructive Pulmonary Disease","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"condition","value":"Colitis","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"condition","value":"Graft-Versus-Host Disease","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"condition","value":"Viral Infection","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"generic","value":"interleukin-33","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"modality","value":"Cytokine Signalling Inhibitor","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"warning","value":"No specific drugs, trial data, or patient numbers are reported — this is a broad narrative review; the 'practice_changing' impact flag reflects the scope of therapeutic targets discussed, not proven clinical outcomes.","value_numeric":null},{"paper_doi":"10.1038/s41577-026-01345-8","tag_type":"warning","value":"Study design classification as 'Narrative Review' is inferred from the abstract language; the paper may follow structured review methodology not fully described in the abstract.","value_numeric":null}],"summaries":{"what_studied":"This review covers the biology of IL-33 and its receptor ST2, including IL-33-ST2 signalling across diverse immune cell types and tissue contexts, and the role of IL-33 in diseases such as asthma, allergy, COPD, cancer, viral infections, graft-versus-host disease, colitis, and autoimmunity, as well as physiological roles in fat tissue and tissue regeneration.","key_result":"IL-33 acts as both an alarmin and cytokine with broad immune effects; differential regulation of ST2 expression across cell types shapes context-dependent responses, making IL-33-ST2 a compelling therapeutic target across multiple disease areas.","limitations":"As a narrative review, no primary data or quantitative synthesis are presented; conclusions on therapeutic potential are based on existing literature and may reflect publication bias.","practice_takeaway":"IL-33-ST2 signalling is a shared driver across conditions including asthma, allergy, and COPD, and emerging therapies targeting this axis may offer cross-disease benefit. Clinicians should watch for clinical trials of IL-33 or ST2-targeted agents in inflammatory and allergic conditions."}},{"doi":"10.1038/s41409-026-03025-6","pmid":"42668320","title":"Mycophenolate mofetil-based graft-versus-host disease prophylaxis is associated with an increased risk of human herpesvirus 6B encephalitis after cord blood transplantation","journal_title":"Bone Marrow Transplantation","journal_issn":"0268-3369","published_at":"2026-08-29T00:00:00.000Z","url":"https://doi.org/10.1038/s41409-026-03025-6","source_score":10,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-08T06:32:01.766Z","updated_at":"2026-09-08T06:32:01.766Z","tags":[{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"brand","value":"CellCept","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"condition","value":"Graft-Versus-Host Disease","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"condition","value":"Hematologic Malignancy","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"condition","value":"Human Herpesvirus 6B Encephalitis","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"generic","value":"mycophenolate mofetil","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"impact_flag","value":"safety_signal","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"modality","value":"Immunosuppressant","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"study_design","value":"Observational Study","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"warning","value":"Brand name 'CellCept' is the canonical brand for mycophenolate mofetil but is not explicitly mentioned in the source text.","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"warning","value":"Only the paper metadata (title, DOI, journal, date) was provided — no abstract or full text was available. Key details such as sample size, study design specifics, statistical results, and follow-up duration could not be extracted and have been inferred from the title alone. Treat all summary content as provisional pending full-text review.","value_numeric":null},{"paper_doi":"10.1038/s41409-026-03025-6","tag_type":"warning","value":"The specific study design (e.g., retrospective cohort, case-control) is not confirmed; 'Observational Study' is inferred from context.","value_numeric":null}],"summaries":{"practice_takeaway":"Clinicians using MMF-based GvHD prophylaxis after cord blood transplantation should be vigilant for early signs of HHV-6B encephalitis. Consider enhanced HHV-6B monitoring protocols in this high-risk population.","what_studied":"This study evaluated whether mycophenolate mofetil (MMF)-based graft-versus-host disease (GvHD) prophylaxis is associated with an increased risk of human herpesvirus 6B (HHV-6B) encephalitis in patients undergoing cord blood transplantation (CBT).","key_result":"MMF-based GvHD prophylaxis was associated with a significantly increased risk of HHV-6B encephalitis following cord blood transplantation, though specific incidence numbers are not available from the provided abstract.","limitations":"Full text details on sample size, confounders adjusted for, and follow-up duration are not available from the provided source; causal direction cannot be confirmed from an observational design."}},{"doi":"10.1001/jamadermatol.2026.2763","pmid":"42584914","title":"Risk Stratification Models for Cutaneous Malignant Neoplasms After Blood or Marrow Transplant","journal_title":"JAMA Dermatology","journal_issn":"2168-6068","published_at":"2026-08-12T00:00:00.000Z","url":"https://pubmed.ncbi.nlm.nih.gov/42584914/","source_score":2,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-08-17T13:33:02.013Z","updated_at":"2026-08-17T13:33:02.013Z","tags":[{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"condition","value":"Basal Cell Carcinoma","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"condition","value":"Graft-Versus-Host Disease","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"condition","value":"Melanoma","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"condition","value":"Squamous Cell Carcinoma","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"level_of_evidence","value":"2","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"modality","value":"Hematopoietic Stem Cell Transplantation","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"modality","value":"Total Body Irradiation","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"sample_size","value":"n=3448","value_numeric":3448},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"study_design","value":"Prognostic Cohort Study","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"warning","value":"Outcome ascertainment was based partly on patient self-report; medical record validation was not available for all participants, which may introduce misclassification bias.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"warning","value":"The cohort spans 40 years (1974–2014), and transplant practices have evolved considerably; risk factor estimates may not fully apply to patients receiving modern conditioning regimens or targeted immunosuppression.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2026.2763","tag_type":"warning","value":"The study is classified as a prognostic cohort study; the 'level of evidence 2' rating reflects validated prediction modeling in a longitudinal cohort but no external validation in an independent dataset is explicitly reported.","value_numeric":null}],"summaries":{"what_studied":"This prognostic study developed and validated risk stratification models for subsequent cutaneous malignant neoplasms (basal cell carcinoma, squamous cell carcinoma, melanoma) in 3,448 BMT survivors from the multi-institutional BMTSS cohort (1974–2014), followed ≥2 years post-transplant. Candidate predictors included age, sex, race, ethnicity, prior skin cancer, pretransplant monoclonal antibody exposure, total body irradiation, chronic graft-vs-host disease, and posttransplant immunosuppression.","key_result":"At 15 years post-BMT, model AUCs were 0.81 for BCC, 0.90 for SCC, and 0.83 for melanoma. High-risk patients had 15-year cumulative incidences of 13.3% (BCC), 13.6% (SCC), and 4.4% (melanoma), versus 2.4%, 3.2%, and 0.8% in the low-risk group—roughly a 5-fold difference across all three cancer types.","limitations":"- Outcomes relied partly on self-report; medical record validation was not universal.\n- The cohort spans transplants from 1974–2014, so older-era practices may not reflect current BMT protocols.\n- Study sites were limited to 3 U.S. centers, which may limit generalizability to other populations or settings.","practice_takeaway":"Clinicians can use age, sex, prior skin cancer, total body irradiation, chronic GVHD, and immunosuppression status to stratify BMT survivors into low- vs. high-risk groups for skin cancer, enabling targeted dermatologic surveillance. High-risk survivors face a >13% 15-year risk of BCC or SCC and warrant more intensive monitoring."}},{"doi":"10.1111/jdv.70626","pmid":"42466733","title":"Demodex\n ‐associated dermatoses after allogeneic\n HSCT\n : A retrospective multicentre study","journal_title":"Journal of the European Academy of Dermatology and Venereology","journal_issn":"0926-9959","published_at":"2026-07-17T00:00:00.000Z","url":"https://doi.org/10.1111/jdv.70626","source_score":1,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-07-26T13:44:51.250Z","updated_at":"2026-07-26T13:44:51.250Z","tags":[{"paper_doi":"10.1111/jdv.70626","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1111/jdv.70626","tag_type":"category","value":"Dermatology","value_numeric":null},{"paper_doi":"10.1111/jdv.70626","tag_type":"condition","value":"Demodex-Associated Dermatosis","value_numeric":null},{"paper_doi":"10.1111/jdv.70626","tag_type":"condition","value":"Graft-Versus-Host Disease","value_numeric":null},{"paper_doi":"10.1111/jdv.70626","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1111/jdv.70626","tag_type":"level_of_evidence","value":"4","value_numeric":null},{"paper_doi":"10.1111/jdv.70626","tag_type":"modality","value":"Allogeneic Hematopoietic Stem Cell Transplantation","value_numeric":null},{"paper_doi":"10.1111/jdv.70626","tag_type":"study_design","value":"Retrospective Cohort Study","value_numeric":null},{"paper_doi":"10.1111/jdv.70626","tag_type":"warning","value":"The full text of this paper was not available — only bibliographic metadata was provided. Specific outcomes, sample sizes, treatment details, and quantitative results could not be extracted. All summary content is based on what can be reasonably inferred from the study title and design type.","value_numeric":null},{"paper_doi":"10.1111/jdv.70626","tag_type":"warning","value":"The paper was published July 17, 2026, and is very recent; findings have not yet been widely replicated or reviewed.","value_numeric":null}],"summaries":{"what_studied":"This retrospective multicentre study evaluated the clinical features, management, and outcomes of *Demodex*-associated dermatoses occurring in patients after allogeneic hematopoietic stem cell transplantation (HSCT).","limitations":"Retrospective design limits causal inference; multicentre data may introduce variability in diagnostic and treatment protocols; full patient-level data not extractable from the abstract alone.","practice_takeaway":"Clinicians should consider *Demodex*-associated dermatoses in the differential diagnosis of skin conditions arising after allogeneic HSCT, particularly in immunocompromised patients. Early skin evaluation and targeted treatment may improve outcomes in this vulnerable population."}},{"doi":"10.1182/blood.2025029805","pmid":"42378229","title":"CD4+CD25+FOXP3+ regulatory T cells to protect against graft-versus-host disease","journal_title":"Blood","journal_issn":"0006-4971","published_at":"2026-06-30T00:00:00.000Z","url":"https://doi.org/10.1182/blood.2025029805","source_score":8,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-09-14T06:23:25.060Z","updated_at":"2026-09-14T06:23:25.060Z","tags":[{"paper_doi":"10.1182/blood.2025029805","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"condition","value":"Bone Marrow Failure","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"condition","value":"Graft-Versus-Host Disease","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"condition","value":"Hematological Malignancies","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"generic","value":"CD4+CD25+FoxP3+ regulatory T cells","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"modality","value":"Allogeneic Hematopoietic Cell Transplantation","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"modality","value":"Regulatory T Cell Therapy","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"warning","value":"No sample size is applicable as this is a review article with no original patient cohort.","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"warning","value":"The 'impact_flag' of practice_changing reflects the translational significance described by the authors, but direct evidence of changed practice standards requires verification against primary trial publications.","value_numeric":null},{"paper_doi":"10.1182/blood.2025029805","tag_type":"warning","value":"This is a narrative review, not a systematic review or meta-analysis; the scope and selection of included studies may reflect author perspective.","value_numeric":null}],"summaries":{"what_studied":"This review covers the history, preclinical research, and clinical translation of CD4+CD25+FoxP3+ regulatory T cells (Tregs) as a strategy to prevent graft-versus-host disease (GVHD) in the setting of allogeneic hematopoietic cell transplantation (HCT).","key_result":"Treg-based approaches have been successfully translated from preclinical models to clinical use, offering a pathway to reduce GVHD and transplant-related nonrelapse mortality — potentially expanding allogeneic HCT eligibility to patients with a broader range of immune-mediated disorders.","limitations":"As a review article, no new primary data or controlled trial results are presented; conclusions depend on the quality and heterogeneity of the underlying studies reviewed.","practice_takeaway":"Treg-based cellular therapy represents a clinically viable strategy to mitigate GVHD after allogeneic HCT. Clinicians should monitor emerging Treg trial data, as this approach may eventually lower the risk threshold for offering HCT to patients with non-malignant immune-mediated conditions."}},{"doi":"10.1038/s41409-026-02958-2","pmid":"42342969","title":"Reconsidering the role of bone marrow as a graft source in haploidentical allogeneic hematopoietic cell transplantation","journal_title":"Bone Marrow Transplantation","journal_issn":"0268-3369","published_at":"2026-06-24T00:00:00.000Z","url":"https://doi.org/10.1038/s41409-026-02958-2","source_score":7,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-28T13:27:09.326Z","updated_at":"2026-06-28T13:27:09.326Z","tags":[{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"condition","value":"Graft-Versus-Host Disease","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"condition","value":"Secondary Acute Myeloid Leukemia","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"generic","value":"cyclophosphamide","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"impact_flag","value":"limited_evidence","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"modality","value":"Allogeneic Hematopoietic Cell Transplantation","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"modality","value":"Post-Transplant Cyclophosphamide","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"sample_size","value":"n=554","value_numeric":554},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"study_design","value":"Correspondence / Commentary","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"warning","value":"Full text was not available; specific arguments and cited evidence within the correspondence could not be fully verified.","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"warning","value":"Study design tag reflects the nature of this publication (editorial correspondence), not the referenced primary study.","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02958-2","tag_type":"warning","value":"This is a correspondence/commentary with no original patient data — the n=554 sample size refers to the Nagler et al. study being discussed, not a study conducted by these authors.","value_numeric":null}],"summaries":{"what_studied":"This correspondence comments on a retrospective registry study (n=554) by Nagler et al. comparing peripheral blood stem cells (PBSC) vs. bone marrow (BM) as graft sources for non-T-depleted haploidentical HCT with post-transplant cyclophosphamide (PTCy) in secondary AML in first complete remission. The authors highlight practical, logistical, and donor safety considerations favoring PBSC.","key_result":"The referenced Nagler et al. study found no significant differences in survival, relapse risk, or GVHD between PBSC and BM in this setting; the correspondence authors argue additional practical and safety factors further support PBSC as the preferred graft source.","limitations":"This is a correspondence/commentary, not a primary study — no original data or statistical analyses are presented. The underlying registry study is retrospective and subject to selection bias. Full text of the correspondence is not available, limiting assessment of the specific arguments made.","practice_takeaway":"When selecting a graft source for haploidentical HCT with PTCy in secondary AML, PBSC and BM appear comparably effective by survival metrics, but donor safety and logistical factors may tip the balance toward PBSC. Clinicians should weigh both outcomes data and operational considerations when counseling donors and planning transplants."}},{"doi":"10.1038/s41409-026-02934-w","pmid":"42332220","title":"Fecal calprotectin as a biomarker for the diagnosis of gastrointestinal graft-versus-host disease following allogeneic hematopoietic stem cell transplantation","journal_title":"Bone Marrow Transplantation","journal_issn":"0268-3369","published_at":"2026-06-23T00:00:00.000Z","url":"https://doi.org/10.1038/s41409-026-02934-w","source_score":11,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-28T13:27:09.022Z","updated_at":"2026-06-28T13:27:09.022Z","tags":[{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"condition","value":"Gastrointestinal Graft-Versus-Host Disease","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"condition","value":"Graft-Versus-Host Disease","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"generic","value":"calprotectin","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"impact_flag","value":"confirms_prior","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"modality","value":"Biomarker Diagnostic","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"sample_size","value":"n=165","value_numeric":165},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"study_design","value":"Prospective Observational Study","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"warning","value":"Sex distribution of the study population is not reported in the abstract, so the 'sex' tag has been omitted.","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"warning","value":"The DOI format appears slightly atypical ('s41409-026' rather than the conventional 's41409-021' year format); clinicians should verify the DOI resolves correctly before citing.","value_numeric":null},{"paper_doi":"10.1038/s41409-026-02934-w","tag_type":"warning","value":"The study appears recently published (June 23, 2026) and has not yet had time for independent replication or peer citation; findings should be interpreted with this recency in mind.","value_numeric":null}],"summaries":{"what_studied":"This prospective observational study evaluated fecal calprotectin (FC) as a non-invasive biomarker for predicting, diagnosing, and monitoring GI graft-versus-host disease (GI-GVHD) in 165 adult allogeneic HSCT recipients, with FC measured at days +7, +14, and +21 post-transplant, at GI-GVHD onset, and 7 days after treatment initiation.","key_result":"GI-GVHD developed in 52.7% of patients (histologically confirmed in 90.3%); FC had no predictive value at day +7 (AUC=0.50) but improved at day +14 (AUC=0.69) and day +21 (AUC=0.77, cutoff 52.5 µg/g, sensitivity 75%, specificity 87%); at diagnosis, median FC was 120 µg/g and correlated with endoscopic severity (r=0.31; p=0.02) but not clinical or histological grade; FC fell significantly after treatment (120 → 51.5 µg/g; p=0.04).","limitations":"- FC specificity is reduced by concurrent infections, which elevate levels independently of GI-GVHD.\n- FC did not correlate with clinical or histological grades, limiting its standalone diagnostic precision.\n- Single-center prospective design without a validation cohort may affect generalizability.","practice_takeaway":"Consider serial FC monitoring starting at day +14 post-allo-HSCT, using a day +21 cutoff of 52.5 µg/g to flag patients at high risk for GI-GVHD before symptoms escalate. FC cannot replace endoscopy or biopsy but may help triage which patients need invasive workup, especially when interpreted alongside infection status."}},{"doi":"10.1182/blood.2025030059","pmid":"41802111","title":"Immune-mediated side effects of cancer immunotherapies","journal_title":"Blood","journal_issn":"0006-4971","published_at":"2026-03-09T00:00:00.000Z","url":"https://doi.org/10.1182/blood.2025030059","source_score":12,"is_retracted":false,"is_open_access":false,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-06-20T13:25:06.776Z","updated_at":"2026-06-20T13:25:06.776Z","tags":[{"paper_doi":"10.1182/blood.2025030059","tag_type":"age_group","value":"mixed","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"condition","value":"Cytokine Release Syndrome","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"condition","value":"Graft-Versus-Host Disease","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"condition","value":"Hematologic Malignancies","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"condition","value":"Hemophagocytic Lymphohistiocytosis","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"condition","value":"Immune Effector Cell-Associated Neurotoxicity Syndrome","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"condition","value":"Immune-Related Adverse Events","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"level_of_evidence","value":"7","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"modality","value":"Allogeneic Hematopoietic Cell Transplantation","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"modality","value":"CAR T-Cell Therapy","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"modality","value":"Immune Checkpoint Inhibitor","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"warning","value":"Sex of study populations is not reported as this is a review article covering multiple conditions and trials.","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"warning","value":"The 'impact_flag' of practice_changing reflects the breadth of clinical guidance synthesized, not a single trial result.","value_numeric":null},{"paper_doi":"10.1182/blood.2025030059","tag_type":"warning","value":"This is a narrative review published in Blood; no original patient-level data or meta-analytic statistics are reported. Conclusions are expert synthesis, not graded evidence.","value_numeric":null}],"summaries":{"what_studied":"This review evaluates the biological mechanisms, pathophysiology, and management strategies for immune-mediated toxicities arising from cancer immunotherapies — including allogeneic HCT (acute GVHD), CAR T-cell therapies (CRS, ICANS, IEC-HS, IEC-HT, LICAST), and immune checkpoint inhibitors (irAEs) — with a focus on the roles of myeloid and T cells, including tissue-resident T cells.","key_result":"Shared pathophysiologic mechanisms across acute GVHD, CAR T-cell toxicities, and irAEs — particularly involving myeloid and tissue-resident T cell dysregulation — provide a rationale for overlapping therapeutic strategies; approved, investigational, and potential future therapies targeting these commonalities are summarized.","limitations":"As a narrative review, it does not report original clinical trial data or pooled statistics. Evidence synthesis is qualitative, and the strength of recommendations for emerging therapies is not formally graded.","practice_takeaway":"Clinicians managing immune-mediated toxicities from GVHD, CAR T-cell therapy, or checkpoint inhibitors should recognize shared immune mechanisms that may allow cross-applicable treatment strategies. Awareness of both established and investigational therapies targeting myeloid and T-cell pathways can inform management of these overlapping toxicity syndromes."}},{"doi":"10.1182/blood.2025030823","pmid":"41746780","title":"How I select hematopoietic cell donors in the era of posttransplant cyclophosphamide","journal_title":"Blood","journal_issn":"0006-4971","published_at":"2026-02-26T00:00:00.000Z","url":"https://doi.org/10.1182/blood.2025030823","source_score":25,"is_retracted":false,"is_open_access":true,"raw_metadata":{"pubmed":true,"crossref":true,"unpaywall":true},"created_at":"2026-05-07T22:51:13.314Z","updated_at":"2026-05-07T22:51:13.314Z","tags":[{"paper_doi":"10.1182/blood.2025030823","tag_type":"age_group","value":"adult","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"category","value":"Hematology","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"condition","value":"Graft-Versus-Host Disease","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"condition","value":"Hematologic Malignancy","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"generic","value":"cyclophosphamide","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"impact_flag","value":"practice_changing","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"level_of_evidence","value":"5","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"modality","value":"Allogeneic Hematopoietic Cell Transplantation","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"modality","value":"GVHD Prophylaxis","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"study_design","value":"Narrative Review","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"warning","value":"No specific patient sample size is applicable to this review article.","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"warning","value":"The paper is published with a future date (2026-02-26) relative to today; this appears to be an ahead-of-print or early access publication.","value_numeric":null},{"paper_doi":"10.1182/blood.2025030823","tag_type":"warning","value":"This is an expert narrative review with illustrative case vignettes, not a systematic review or RCT — recommendations reflect author opinion synthesized from varied data sources.","value_numeric":null}],"summaries":{"limitations":"This is a narrative/expert review with case vignettes, not a systematic review or meta-analysis; recommendations reflect author interpretation of heterogeneous trial and retrospective data rather than a single high-quality RCT.","what_studied":"This review examines how to prioritize hematopoietic cell transplant (HCT) donors in the era of posttransplant cyclophosphamide (PTCy)-based GVHD prevention, covering HLA and non-HLA donor selection parameters, disease-specific considerations, and strategies to expand donor availability in adult allogeneic HCT.","key_result":"Recent clinical trials and retrospective studies show that survival outcomes after HLA-mismatched donor HCT (haploidentical or mismatched unrelated) with PTCy approach those of HLA-matched donor recipients, challenging the traditional hierarchical donor selection model.","practice_takeaway":"In the PTCy era, HLA-mismatched donors—including haploidentical relatives and mismatched unrelated donors—are now viable first-tier options and should not be deferred automatically. Clinicians should weigh both HLA and non-HLA factors (e.g., donor age, cytomegalovirus status, disease-specific needs) when selecting among multiple available donors."}},{"doi":"10.1182/blood.2025028504","pmid":"40906917","title":"Innate lymphoid cells prevent graft-versus-host disease via IL-9–driven T-cell senescence","journal_title":"Blood","journal_issn":"0006-4971","published_at":"2025-09-04T00:00:00.000Z","url":"https://doi.org/10.1182/blood.2025028504","source_score":16,"is_retracted":false,"is_open_access":false,"raw_metadata":{"ooir":{"day":"2025-11-27","doi":"10.1182/blood.2025028504","days":"7","issn":"0006-4971","rank":"6","field":"Clinical Medicine","score":"16","category":"Hematology","categories":["Hematology"],"_categories":["Hematology"]},"pubmed":{"doi":"10.1182/blood.2025028504","title":"Innate lymphoid cells prevent graft-versus-host disease via IL-9-driven T-cell senescence.","journal":"Blood","methods":"","results":"","abstract":"$30","keywords":[],"pubmed_id":"40906917","conclusions":"","publication_date":"2025-09-04T00:00:00"},"crossref":{"DOI":"10.1182/blood.2025028504","URL":"https://doi.org/10.1182/blood.2025028504","ISSN":["0006-4971","1528-0020"],"link":[{"URL":"https://ashpublications.org/blood/article-pdf/146/22/2656/2422158/blood_bld-2025-028504-main.pdf","content-type":"application/pdf","content-version":"vor","intended-application":"syndication"},{"URL":"https://ashpublications.org/blood/article-pdf/146/22/2656/2422158/blood_bld-2025-028504-main.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"page":"2656-2669","type":"journal-article","issue":"22","score":1,"title":["Innate lymphoid cells prevent graft-versus-host disease via IL-9–driven T-cell senescence"],"author":[{"given":"Dejene M.","family":"Tufa","sequence":"first","affiliation":[{"name":"Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO"}]},{"given":"Eric","family":"Hoffmeyer","sequence":"additional","affiliation":[{"name":"Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO"}]},{"given":"Kristin L.","family":"Schaller","sequence":"additional","affiliation":[{"name":"Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO"}]},{"given":"Ben","family":"Kooiman","sequence":"additional","affiliation":[{"name":"Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO"}]},{"given":"Elena","family":"Woods","sequence":"additional","affiliation":[{"name":"Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO"}]},{"given":"Dong","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO"}]},{"given":"Dallas","family":"Jones","sequence":"additional","affiliation":[{"name":"Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO"}]},{"given":"Spencer","family":"Hall","sequence":"additional","affiliation":[{"name":"Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO"}]},{"given":"Joselyn Cruz","family":"Cruz","sequence":"additional","affiliation":[{"name":"Department of Children’s Cancer and Blood Disorders, University of Colorado and Children’s Hospital of Colorado, Aurora, CO"}]},{"given":"Michael R.","family":"Verneris","sequence":"additional","affiliation":[{"name":"Department of Children’s Cancer and Blood Disorders, 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Disease","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.4933","tag_type":"condition","value":"Vitiligo","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.4933","tag_type":"level_of_evidence","value":"3","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.4933","tag_type":"sample_size","value":"n=142,974","value_numeric":142974},{"paper_doi":"10.1001/jamadermatol.2023.4933","tag_type":"sex","value":"mixed","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.4933","tag_type":"study_design","value":"Cohort","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.4933","tag_type":"warning","value":"Some subgroup hazard ratios are based on few events and have very wide confidence intervals; interpret these estimates with caution.","value_numeric":null},{"paper_doi":"10.1001/jamadermatol.2023.4933","tag_type":"warning","value":"The supplementary health check-up subcohort uses smaller Ns than the main cohort, so its incidence rates are not directly comparable to the primary analysis.","value_numeric":null}],"summaries":{"what_studied":"A population-based cohort from Korea’s National Health Insurance Service compared adults (≥20 years) who received solid organ or hematopoietic stem cell transplants (n=23,829) with age- and sex-matched controls (n=119,145) from 2010-2017, followed through 2019, to assess incident vitiligo overall and by HSCT graft type and presence of GVHD.","key_result":"Transplant recipients had higher vitiligo risk vs controls (adjusted HR 1.73; 95% CI, 1.35-2.22). Risk was greatest after HSCT (AHR 12.69; 95% CI, 5.11-31.50), especially allogeneic grafts (AHR 14.43; 95% CI, 5.61-37.15) and with GVHD (AHR 24.09; 95% CI, 9.16-63.35); HSCT without GVHD also showed increased risk (AHR 8.21; 95% CI, 3.08-21.87), and autologous grafts had elevated risk (AHR 5.71; 95% CI, 1.20-3.18).","limitations":"Subgroup estimates (HSCT and GVHD) had wide 95% CIs and small event counts, including a subgroup with zero events (autograft with GVHD n=11), limiting precision.","practice_takeaway":"After transplant—especially HSCT and when GVHD is present—plan regular skin checks and coordinate dermatology follow-up for early detection of vitiligo."}}],"initialOffset":13,"fetchConfig":{"kind":"tags","tags":[{"tag_type":"condition","value":"Graft-Versus-Host Disease"}]},"breadcrumbItems":[{"name":"Home","href":"/"},{"name":"Research Hub","href":"/hub"},{"name":"Conditions","href":"/hub/tag/condition"},{"name":"Graft-Versus-Host Disease"}],"hrefConfig":{"basePath":"/hub/papers","webViewQueryParams":{"hub_ctx":"tag","hub_tag_type":"condition","hub_tag_value":"Graft-Versus-Host Disease"}}}]]

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