Journal of Clinical Immunology最新文献

{"title":"A Cohort Study of 38 Classic Wiskott-Aldrich Syndrome Cases with Six Novel Mutations.","authors":"Anahita Razaghian, Mohsen Badalzadeh, Amir Ali Hamidieh, Raheleh Shokouhi Shoormasti, Nasrin Behniafard, Massoud Houshmand, Leila Moradi, Samin Alavi, Maryam Behfar, Masoud Movahedi, Mohammad Gharagozlou, Tahereh Rostami, Farideh Moussavi, Morteza Fallahpour, Mansoureh Shariat, Nima Parvaneh, Alireza Shafiei, Hamid Ahanchian, Delara Babaei, Mohammad Hassan Bemanian, Roshanak Radmehr, Reyhaneh Khademi, Somayeh Shamlou, Mohammad Reza Fazlollahi, Zahra Pourpak","doi":"10.1007/s10875-026-01986-3","DOIUrl":"10.1007/s10875-026-01986-3","url":null,"abstract":"<p><p>PURPOSE: Wiskott-Aldrich syndrome (WAS) is an X-linked immunodeficiency characterized by eczema, microthrombocytopenia, and recurrent infections. This study evaluates the frequency of clinical manifestations and overall outcomes in WAS patients, comparing those who received hematopoietic stem cell transplantation (HSCT) with those who did not. METHODS: Thirty-eight boys with a definite diagnosis of WAS were retrospectively evaluated in the Immunology, Asthma, and Allergy Research Institute registry in Tehran from 2006 to 2023. RESULTS: The median ages at symptom onset, diagnosis, and delay to diagnosis were 3.5, 7.5, and 4.5 months, respectively. The clinical presentations include allergies in 38 (100%), infection in 37 (97.4%), hemorrhage in 36 (94.7%), autoimmunity in 14 (36.8%), and malignancies or myelodysplasia syndrome in 3 (7.9%) patients. Although microthrombocytopenia is a hallmark of WAS, 34.4% of our cases had normal platelet size. The WAS gene analysis in 36 of 38 patients identified six novel mutations. Sixteen patients underwent HSCT. Disease-free survival was reported in 10 (62.5%) of them, whereas 6 (37.5%) of them were deceased. The mortality rate in non-transplant patients was 15/22 (68.2%). CONCLUSION: Most WAS patients experienced atopy, recurrent infections, and bleeding. Moreover, autoimmunity and malignancies have increased relative to the general population. Moreover, the mortality rate is high, especially among those who did not receive HSCT. Keeping in mind that thrombocytopenia alongside eczema and/or infection in a male infant can be the presentation of this fatal disease. Early diagnosis and treatment could be lifesaving and prevent severe morbidities. </p>","PeriodicalId":15531,"journal":{"name":"Journal of Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12975855/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146258273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Good's Syndrome Mirrors a Combined Immunodeficiency with Anti-Cytokine Antibodies in the Total Absence of B Cells.","authors":"Aunonna Kabir, Louise Gilbert, Dornaz Almasizadeh, Reza Alizadehfar, Vanessa Polito, David Langlais, René P Michel, Christos M Tsoukas","doi":"10.1007/s10875-026-01992-5","DOIUrl":"10.1007/s10875-026-01992-5","url":null,"abstract":"<p><p>Good’s Syndrome, an adult-onset immune deficiency, has been traditionally grouped with humoral immune deficiencies such as Common Variable Immune Deficiency (CVID) and X-linked agammaglobulinemia (XLA) despite the unique presence of the thymic neoplasm, late age of onset, frequent opportunistic infections and multiple cytopenias. Low prevalence and sporadic reporting have limited investigative efforts. We conducted a prospective, multimodal, study to establish the GS phenotype in the absence of severe infections. A previously characterized cohort of GS patients was compared to healthy individuals and those diagnosed with CVID or XLA using serology, immunophenotyping and histopathology. We also attempted to establish an inborn cause of the immune deficiency with HLA typing and Whole Exome Sequencing. GS patients exhibited severe hypogammaglobulinemia, a complete absence of B-cells in the peripheral blood and in biopsied primary and secondary lymphoid tissues. Total lymphocytes and CD4 T-cell counts were markedly reduced in GS but with intact T-cell proliferative capacity to in vitro mitogen and lectin stimulation. Autoantibody profiling identified high titers of antibodies in GS patient plasma to several cytokines, notably anti-interferons, which persisted for several years. These antibodies overlapped with those observed in thymoma patients without GS. We demonstrate that GS involves profound B-cell-loss, extending beyond blood to the lymphoid tissue, however plasma cells and circulating anti-cytokine antibodies can persist for years. In the absence of a unifying monogenic defect, the findings are suggestive of a thymoma-associated breakdown in central tolerance driving the immune dysregulation and deficiency seen in GS.</p>","PeriodicalId":15531,"journal":{"name":"Journal of Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12967467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146213354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spectrum of Primary Immune Regulatory Disorders in Children in a Highly Consanguineous Population: Report from a National Registry.","authors":"Amal Alajmi, Sondus Alsharidah, Nisreen Khalifa, Ahmed Elhussein, Ahmad Al-Khabaz, Ahmad Alaqeel, Waleed Al-Herz","doi":"10.1007/s10875-026-01993-4","DOIUrl":"10.1007/s10875-026-01993-4","url":null,"abstract":"<p><p>BACKGROUND: Primary Immune Regulatory Disorders (PIRDs) are caused by genetic defects resulting in diverse clinical manifestations. We aimed to present the spectrum of PIRDs in children in Kuwait. METHODS: The data was obtained from the Kuwait National Primary Immunodeficiency Disorders Registry (KNPIDR), and the patients were followed prospectively. RESULTS: 59 patients with PIRDs, constituting 14% of all patients registered in the KNPIDR, were included in this study. Most of the patients belonged to familial hemophagocytic lymphohistiocytosis syndromes (42.4%), followed by regulatory T cell defects subcategories (15.3%). The median ages at the onset of symptoms and diagnosis were 4 and 18 months, respectively. Parental consanguinity was documented in 88.1% of cases while family history of PIRDs in 45.7%. The most common clinical features were lymphoproliferation, hematologic manifestations, and infections, affecting 71.2%, 67.8%, and 47.5%, respectively. Genetic diagnosis was reached in 84.9% of the tested patients and the most common genes affected were STXBP2 followed by PRF1 and LYST. Most patients (88.8%) had autosomal recessive disease. 35.6% of the patients underwent hematopoietic stem cell transplantation and a similar percentage received immunosuppressive and/or immunomodulating therapies. There was a total of 21 deaths (35.6%) with a median age at death of 36 months while the median time from diagnosis to death was 5 months. CONCLUSIONS: PIRDs are heterogenous group of disorders with complex disease phenotypes. Genetic testing should be done as soon as possible when these diseases are suspected since early diagnosis is crucial for proper therapeutic interventions. </p>","PeriodicalId":15531,"journal":{"name":"Journal of Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12960471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146194735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WAS Protein Deficiency Disrupts Memory B Cell Formation During Acute LCMV Infection.","authors":"Liang Zhang, Yongjie Liu, Dujuan Zhou","doi":"10.1007/s10875-026-01984-5","DOIUrl":"10.1007/s10875-026-01984-5","url":null,"abstract":"<p><p>Wiskott-Aldrich syndrome (WAS) is a rare x-linked monogenic immunodeficiency disease, caused by the mutation of WAS gene encoding WAS protein (WASp). Previous findings in WAS patients show B cell perturbations in the periphery, characterized by diminished B-cell numbers and phenotype abnormalities, including reduced frequency of classical CD27⁺ memory B cells (MBCs), accompanied by an unusual expansion of atypical CD21low MBCs. The mechanism underlying these abnormalities in MBCs developmental pathway has not been completely dissected. In this study, WASp knock-out mice undergone with acute lymphocytic choriomeningitis virus (LCMV) infection was used as a model to investigate the effects of WASp deficiency on the differentiation of MBCs and the possible mechanisms. We found that by day 11 after infection, the proportion of classical IgG2c⁺ MBCs was dramatically decreased, this was accompanied by a corresponding increase in the proportion of atypical CD21low MBCs. Using single-cell RNA sequencing (scRNA-seq), we also identified WASp deficiency promoted the formation of atypical MBCs during acute viral infection. Remarkably, our study revealed a marked reduction of WASp expression in atypical MBCs. Overall, our data show that WASp is differentially expressed in MBCs subsets, and manipulates the fate of MBCs during acute LCMV infection.</p>","PeriodicalId":15531,"journal":{"name":"Journal of Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12950028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146157287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcatheter Arterial Approach for Refractory Liver Abscesses in Chronic Granulomatous Disease: A Case Series.","authors":"Elisa Profeti, Stefania Ferradino, Lorenza Romani, Gioacchino Andrea Rotulo, Paolo Palma, Gian Luigi Natali, Andrea Finocchi","doi":"10.1007/s10875-025-01976-x","DOIUrl":"10.1007/s10875-025-01976-x","url":null,"abstract":"","PeriodicalId":15531,"journal":{"name":"Journal of Clinical Immunology","volume":"46 1","pages":"16"},"PeriodicalIF":5.7,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12891042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146149980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pediatric IPEX-Associated Dermatitis Responds To Dupilumab: Evidence from Skin Transcriptomics and Immune Profiling.","authors":"Jinxiang Yang, Guofang Li, Jiayan Zhang, Jiao Wang, Yijun Yang, Qiuyang Guo, Kexin Yan, Haoyang Hu, Jiayi Xue, Yiming Ma, Jianying Liang, ZhiRong Yao, Hui Zhang, Chunxiao Li","doi":"10.1007/s10875-025-01979-8","DOIUrl":"10.1007/s10875-025-01979-8","url":null,"abstract":"<p><strong>Purpose: </strong>Immunodysregulation, Polyendocrinopathy, Enteropathy, and X-linked (IPEX) syndrome is a rare autoimmune disorder caused by mutations in the FOXP3 gene. Patients with IPEX frequently present with severe dermatitis, diabetes, and enteropathy. This study explores the efficacy of Dupilumab (an anti-IL-4Rα monoclonal antibody) in treating persistent, severe dermatitis in an IPEX patient refractory to conventional treatments like sirolimus.</p><p><strong>Methods: </strong>We conducted a clinical case study of a 2-year-old IPEX patient with refractory dermatitis. Whole-exome sequencing (WES) confirmed the FOXP3 mutation. Skin biopsies were analyzed for inflammatory gene expression by RNA sequencing and immunohistochemistry to characterize inflammatory pathways. Immune cell phenotyping was performed using flow cytometry pre- and post-treatment in peripheral blood mononuclear cells (PBMCs). The patient was treated with Dupilumab alongside sirolimus and prednisone. Clinical improvements were evaluated using the Eczema Area and Severity Index (EASI) score.</p><p><strong>Results: </strong>Immunohistochemistry revealed elevated IL-13 expression. RNA sequencing of skin samples revealed upregulation of both Th1- and Th2-related genes, suggesting a dual inflammatory phenotype in IPEX dermatitis. The patient exhibited significant clinical improvement after 8 months of sustained Dupilumab therapy, with the EASI decreasing from 24.8 to 0.4. Flow cytometry demonstrated a reduction in Th1 and Th2 cell subsets post-treatment, accompanied by an increase in Treg and Th3 cell populations as well as enhanced expression of immunosuppressive markers such as CTLA-4 and CD39.</p><p><strong>Conclusion: </strong>Dupilumab appears promising as a therapeutic option for managing refractory dermatitis in IPEX, particularly by attenuating Th1/Th2 inflammation and promoting regulatory responses mediated by Treg and Th3 cells.</p>","PeriodicalId":15531,"journal":{"name":"Journal of Clinical Immunology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12923480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131930","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"αβT/CD19-depleted Allogeneic Stem Cell Transplantation in Adults with Inborn Errors of Immunity.","authors":"Janneke J H de Winter, Birtan M Ibrahimov, Frances A Verheij, Iris D Brinkman, Anniek H G Stuut, Pleun Schonewille, Marloes W Heijstek, Anna van Rhenen, Lotte E van der Wagen, Laura G M Daenen, Anke Janssen, Tim J A Hutten, Jürgen Kuball, Helen L Leavis, Moniek A de Witte","doi":"10.1007/s10875-025-01978-9","DOIUrl":"10.1007/s10875-025-01978-9","url":null,"abstract":"<p><strong>Purpose: </strong>Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is successful in pediatric patients with inborn errors of immunity (IEI), but its use in adults is complicated by pre-existing organ damage and increased risk of treatment-related mortality. Ex vivo graft engineering using αβTCR/CD19 depletion has shown promising safety profiles in pediatric IEI, yet evidence in adults is limited. We assessed the feasibility and outcomes of αβTCR/CD19-depleted allo-HSCT in adults with IEI, focusing on engraftment, immune reconstitution, and clinical outcomes.</p><p><strong>Methods: </strong>We included 9 adults with IEI and 1 with VEXAS (age 21-51). IEIs included CTLA4HI, APDS, DOCK8, ALPS, DADA2, CVID2, and HA20, with Immune Deficiency and Dysregulation Activity (IDDA) scores of 17-92. αβTCR/CD19-depleted allografts from related, unrelated or haplo-identical donors were used after antithymocyte globulin (ATG) and myeloablative conditioning (thiotepa, melphalan, and fludarabine). Post-transplant immunoprophylaxis included mycophenolate mofetil; 4/10 patients received additional transplant-associated immunosuppression.</p><p><strong>Results: </strong>All patients achieved primary engraftment. One patient with secondary rejection successfully underwent a second allo-HSCT. 5 patients developed grade 2-4 acute GvHD; no chronic GvHD was observed. One patient with GvHD died from COVID-19. All remaining 9 patients were successfully tapered off immunosuppression and showed improved IDDA scores. At 6 months NK, γδT, B and CD8 + T cells normalized; CD4 + numbers reached 149 cells/µl at 1 year. Most patients were successfully vaccinated and could stop immunoglobulin substitution.</p><p><strong>Conclusion: </strong>In conclusion, ex vivo graft engineering using αβTCR/CD19 depletion was feasible in adults with IEI. Clinical outcomes are encouraging, but need to be confirmed in larger studies.</p>","PeriodicalId":15531,"journal":{"name":"Journal of Clinical Immunology","volume":" ","pages":"21"},"PeriodicalIF":4.1,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12913266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146113419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Follicular Helper T Cells and B Cell Maturation in Patients with 22q11.2 Deletion Syndrome and Recurrent Infections.","authors":"Nouf Alsaati, Katherine Beigel, Kelly Maurer, Sarah E Henrickson, Montana Knight, Audrey Green, Victoria Giunta, Daniel E McGinn, Bekah Wang, T Blaine Crowley, Donna M McDonald-McGinn, Kathleen E Sullivan","doi":"10.1007/s10875-026-01987-2","DOIUrl":"10.1007/s10875-026-01987-2","url":null,"abstract":"<p><strong>Purpose: </strong>22q11.2 Deletion Syndrome has been primarily described as a disorder of T cell production secondary to thymic hypoplasia. However, there is great complexity in the clinical picture with infections, autoimmunity, and inflammation occurring. Emerging evidence suggests that qualitative T cell dysfunction occurs, and the goal of this study was to utilize single-cell RNA-seq to better define altered gene expression patterns to inform on the mechanisms associated with recurrent infections.</p><p><strong>Methods: </strong>We utilized single-cell RNA-seq to define distinct populations in 22q11.2 Deletion Syndrome (N = 13) and controls (N = 11) as well as within a subcohort of patients with 22q11.2 Deletion Syndrome and recurrent infections.</p><p><strong>Results: </strong>When we analyzed differentially expressed genes, we identified a signature of type I interferons across all cell types. Within the T cell compartment, and particularly within the follicular helper T cells, we identified a senescence signature. The alterations found in T cells were most substantial in the patients with recurrent infection.</p><p><strong>Conclusions: </strong>While T cell numbers can often normalize in patients with 22q11.2 Deletion Syndrome, our data indicate significantly altered function as defined by differentially expressed genes and aligned with what is known about T cell senescence. The effect was greatest in the patients with recurrent infection. This would be expected to impact T cell function and may account for ongoing symptoms, reduced B cell maturation, and possibly the risk of immune dysregulation.</p>","PeriodicalId":15531,"journal":{"name":"Journal of Clinical Immunology","volume":" ","pages":"20"},"PeriodicalIF":4.1,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12913360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146105811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Partial Purine Nucleoside Phosphorylase Deficiency: an Unexpected Diagnosis in an Adult Patient.","authors":"Manisha Ahuja, Lynette Fairbanks, Catherine Stroud, Andrew Schaefer, Suzanne Elizabeth Elcombe","doi":"10.1007/s10875-025-01941-8","DOIUrl":"10.1007/s10875-025-01941-8","url":null,"abstract":"","PeriodicalId":15531,"journal":{"name":"Journal of Clinical Immunology","volume":"46 1","pages":"14"},"PeriodicalIF":5.7,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12864346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146105734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NET Biomarkers in COVID-19 and Post-COVID Syndrome: a Comprehensive Analysis.","authors":"Diana M Monsalve, Laura Numpaque-Morales, Manuel Rojas, Yeny Acosta-Ampudia, Carolina Ramírez-Santana","doi":"10.1007/s10875-026-01980-9","DOIUrl":"10.1007/s10875-026-01980-9","url":null,"abstract":"<p><p>SARS-CoV-2 triggers immune responses, including neutrophil activation and neutrophil extracellular trap (NET) release, contributing to COVID-19 severity. A significant proportion of patients experience persistent or new symptoms after recovery, referred to as post-COVID syndrome (PCS), which may be associated with NET release persistence. This study aimed to investigate whether NET-related biomarkers remain elevated after acute SARS-CoV-2 infection and to explore their association with PCS. We conducted an analytical descriptive cohort study including patients with acute COVID-19 (n = 35), PCS (n = 35), and a pre-pandemic healthy control group (PPC; n = 35). Serum samples from participants were used to measure NET biomarkers, including MPO-DNA complexes, elastase-DNA complexes, and MPO levels. The capacity to induce NETosis in vitro was evaluated by incubating neutrophils with participant serum. Additionally, soluble immune markers, including cytokines, anti-SARS-CoV-2 antibodies, and autoantibodies, were assessed. A NETosis-based model was developed using NET biomarkers to distinguish between acute COVID-19 or PCS patients and PPC individuals. Our findings revealed a significant increase in NET biomarkers during acute COVID-19 that persisted in PCS. This pattern was consistent with the in vitro study, where sera from PCS patients induced NET release. Additionally, NET biomarkers correlated with neutrophil counts, cytokines, autoantibodies, and inflammatory markers during acute COVID-19 and PCS. The multivariate model of NET biomarkers exhibited a high accuracy in distinguishing acute COVID-19 with an area under the curve (AUC) of 0.99 (CI = 0.98–1.00) and PCS patients with an AUC of 0.91 (CI = 0.84–0.99) from PPC. These findings suggest that persistent NETosis may contribute to PCS pathophysiology, highlighting NETs as potential biomarkers and therapeutic targets in post-viral syndromes.</p>","PeriodicalId":15531,"journal":{"name":"Journal of Clinical Immunology","volume":" ","pages":"19"},"PeriodicalIF":4.1,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12909450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146105814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}