Clinical immunology最新文献

{"title":"Staphylococcus aureus induces miR-21 expression to promote bacterial persistence during nasal colonisation","authors":"Alanna M. Kelly ,&nbsp;Emilio G. Vozza ,&nbsp;Brenda Morris ,&nbsp;Seán C. Cahill ,&nbsp;Charlotte M. Leane ,&nbsp;Sinéad C. Corr ,&nbsp;Rachel M. McLoughlin","doi":"10.1016/j.clim.2025.110593","DOIUrl":"10.1016/j.clim.2025.110593","url":null,"abstract":"<div><div><em>Staphylococcus aureus</em> nasal colonisation is commonplace among healthy individuals, yet the immune mechanisms enabling bacterial persistence remain unclear. <em>S. aureus</em> drives local immunosuppression during nasal colonisation to facilitate persistence. This study reveals that <em>S. aureus</em> subverts microRNA-21 activity to promote IL-10 production within nasal tissue, while simultaneously impeding local pro-inflammatory responses. MiR-21 activity helps establish a <em>S. aureus</em>-induced immunosuppressive microenvironment, which supports <em>S. aureus</em> persistence. Macrophages, which are key IL-10 producers, rapidly upregulate miR-21 upon <em>S. aureus</em> exposure. MiR-21 expression also coincides with an increase in intracellular survival of <em>S. aureus</em> within macrophages. Furthermore, <em>S. aureus</em> represses macrophage glycolysis to promote intracellular survival, which is dependent upon miR-21. Upon <em>S. aureus</em> colonisation, miR-21^−/− mice demonstrate an overall improved bacterial clearance compared to their wild-type counterparts. These findings highlight the targeting of miR-21, which controls glycolytic activity in macrophages, as a potential avenue to reducing bacterial persistence during <em>S. aureus</em> colonisation.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110593"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efgartigimod versus standard of care in new-Onset AChR subtype generalized myasthenia gravis: A prospective cohort study","authors":"Dingxian He ,&nbsp;Lei Jin ,&nbsp;Shuangshuang Wang ,&nbsp;Huahua Zhong ,&nbsp;Hongxi Chen ,&nbsp;Hongyu Zhou ,&nbsp;Zhangyu Zou ,&nbsp;Chongbo Zhao ,&nbsp;Xiao Huan ,&nbsp;Jie Song ,&nbsp;Jianying Xi ,&nbsp;Chong Yan ,&nbsp;Sushan Luo","doi":"10.1016/j.clim.2025.110587","DOIUrl":"10.1016/j.clim.2025.110587","url":null,"abstract":"<div><div>Efgartigimod (EFG) is usually used to treat generalized myasthenia gravis (gMG) with long disease duration; the benefit in new-onset gMG remained unknown. This study included 87 new-onset gMG patients who received either oral steroid and immunosuppressive treatment (Conventional group, <em>n</em> = 30) or combined with EFG (EFG group, <em>n</em> = 57). The primary outcome was minimal symptom expression (MSE) responders, as denoted by a Myasthenia Gravis Activities of Daily Living (MG-ADL) of 0 or 1 for over 4 weeks. At 12 weeks, the proportion of MSE responders was significantly higher in the EFG group (45.61 %, 26/57 vs. 13.33 %, 4/30, <em>p</em> = 0.0026). With the EFG group, patients with late-onset gMG had greater reductions in MG-ADL than those associated with thymoma (7.06 ± 3.25 vs. 4.96 ± 3.40, <em>p</em> = 0.040). EFG may be a promising treatment for rapid disease control in new-onset gMG, but future studies are still required to assess the cost-effectiveness and long-term safety.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110587"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144893349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel pathogenic MAN2B2 variants cause systemic lupus erythematosus and dysregulated glycosylation","authors":"Cheng Gong ,&nbsp;Changming Zhang ,&nbsp;Xu Han ,&nbsp;Ying Jin ,&nbsp;Yangyang Zhang ,&nbsp;Chenlu Liu ,&nbsp;Qintao Wang ,&nbsp;Jiahui Zhang ,&nbsp;Cheng Guo ,&nbsp;Qing Zhou ,&nbsp;Xiaomin Yu ,&nbsp;Zhihong Liu","doi":"10.1016/j.clim.2025.110578","DOIUrl":"10.1016/j.clim.2025.110578","url":null,"abstract":"<div><div>Genetic factors have been demonstrated to play essential roles in the pathogenesis of systemic lupus erythematosus (SLE). Identifying novel disease-causing genes of SLE helps to reveal its molecular mechanisms and new therapeutic targets. In this study, we identified biallelic loss-of-function variants of <em>MAN2B2</em> gene in five unrelated SLE patients by whole exome sequencing. They were characterized by autoimmunity, glomerulonephritis, leukopenia, and immune dysregulation. All variants were absent or ultrarare in population databases and predicted to be damaging by multiple <em>in silico</em> tools. Functional study showed that all the identified variants resulted in complete or partial enzymatic activity loss. Analyses of MAN2B2 knockout HEK293T cells, patient-derived induced pluripotent stem cells (iPSCs) and serum samples revealed defects in glycan degradation and N-glycosylation. The patients exhibited enhanced inflammatory signatures, especially the type I interferon and NF-κB pathways. Mechanically, MAN2B2 deficiency leads to dysregulation of unfolded protein response (UPR) upon endoplasmic reticulum stress, resulting in enhanced expression of inflammatory cytokines. Our findings broaden the genetic etiology spectrum of SLE and identify MAN2B2 as a pivotal regulator in maintaining immune homeostasis, paving the way for innovative diagnostic approaches and molecular pathway-specific therapeutic interventions.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110578"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144854759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural and functional characteristics of local immune memory formation in SARS-CoV-2-infected cynomolgus macaques","authors":"Dong-Yeon Kim ,&nbsp;Green Kim ,&nbsp;Taehwan Oh ,&nbsp;YoungMin Woo ,&nbsp;Bon-Sang Koo ,&nbsp;Seung Ho Baek ,&nbsp;Eun-Ha Hwang ,&nbsp;Gukhui Min ,&nbsp;You Jung An ,&nbsp;Jinyoung Won ,&nbsp;Youngjeon Lee ,&nbsp;Kyung Seob Lim ,&nbsp;Yujin Kim ,&nbsp;Choong-Min Ryu ,&nbsp;Victor Nizet ,&nbsp;Jung Joo Hong","doi":"10.1016/j.clim.2025.110589","DOIUrl":"10.1016/j.clim.2025.110589","url":null,"abstract":"<div><div>As the primary interface with the environment, the lungs require a robust local immune defense against pathogens. In a non-human primate model of SARS-CoV-2 Omicron infection, we used scRNA-seq, spatial transcriptomics, and immunoassays to investigate localized immune memory. Our results demonstrated established adaptive responses in lung tissue and medLNs, with significant activation of tissue-resident T cells and GC (germinal center) B cells. Inducible bronchus-associated lymphoid tissue (iBALT) formed a functional tertiary lymphoid structure, suggesting potential involvement in local immune responses. These findings highlight the pivotal role of local immunity in preventing re-infection and can facilitate targeted mucosal vaccine development.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110589"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144925321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pocapavir treatment of enterovirus encephalitis in a patient with X-linked Agammaglobulinemia","authors":"Annarosa Soresina ,&nbsp;Jessica Galli ,&nbsp;Irene Bellicini ,&nbsp;Silvia Gambara ,&nbsp;Rosaria Scaduto ,&nbsp;Sara Roversi ,&nbsp;Alessandra Tozzo ,&nbsp;Nardo Nardocci ,&nbsp;Lorenzo Pinelli ,&nbsp;Jeff Hincks ,&nbsp;Elisa Fazzi ,&nbsp;Raffaele Badolato","doi":"10.1016/j.clim.2025.110592","DOIUrl":"10.1016/j.clim.2025.110592","url":null,"abstract":"<div><div>We report the case of a young boy with X-linked agammaglobulinemia (XLA) who developed progressive gait instability and postural difficulties. Initial cerebrospinal fluid (CSF) analyses and viral PCR testing were negative; however, a brain biopsy confirmed chronic enteroviral encephalitis. The patient was treated with two compassionate-use cycles of pocapavir, in combination with ongoing high-dose intravenous immunoglobulin (IVIG) therapy. Treatment was well tolerated and led to partial neurological improvement followed by clinical stabilization. This case highlights the diagnostic challenges of enteroviral encephalitis in immunocompromised patients and suggests that investigational antivirals such as pocapavir may offer therapeutic benefit in selected cases.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110592"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144907450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical, biochemical, and genetic characterization of Lebanese patients with chronic granulomatous disease due to NCF2 pathogenic variants","authors":"Youmna El-Orfali ,&nbsp;Hagop Mardirossian ,&nbsp;Habib Al-Kalamouni ,&nbsp;Zeinab El-Zein ,&nbsp;Samar Dalle ,&nbsp;Dima Khreis ,&nbsp;Amani Haddara ,&nbsp;Rima Hanna-Wakim ,&nbsp;Ghassan Dbaibo ,&nbsp;Michel J. Massaad","doi":"10.1016/j.clim.2025.110596","DOIUrl":"10.1016/j.clim.2025.110596","url":null,"abstract":"<div><div>Chronic Granulomatous Disease (CGD) is caused by mutations in the NADPH oxidase complex that impair the ability of phagocytes to eliminate injested pathogens. As a result, patients with CGD suffer from recurrent infections and chronic inflammation. We report the clinical, biochemical, and genetic basis of the disease in 17 CGD patients from Lebanon. Whole exome sequencing (WES) identified 2 distinct mutations in <em>NCF2</em> resulting in the deletion of exons 3 and 5, accounting for 82 % of the cases that underwent WES. This high prevalence provided the rationale for a diagnostic strategy involving assessment of NADPH oxidase function, identification of the affected protein, and targeted gene sequencing. Using this approach, 3 additional CGD patients with simmilar deletions were identified, supporting the presence of a founder effect in the Lebanese population. This biochemical and tageted sequencing approach is rapid, reliable, and cost-effective, making it a particularly valuable diagnostic option for families who cannot afford WES.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110596"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145007608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"“Identification of an antibody against a novel peptide from Porphyromonas gingivalis as a biomarker for rheumatoid arthritis”","authors":"Yung-Ju Yeh ,&nbsp;Hsin-Yi Peng ,&nbsp;Ting-Yin Xue ,&nbsp;Wei-Jing Li ,&nbsp;Po-Hao Huang ,&nbsp;Kai-Jieh Yeo ,&nbsp;Chien-Chung Huang ,&nbsp;Jiunn-Horng Chen ,&nbsp;Chung-Ming Huang ,&nbsp;Der-Yuan Chen ,&nbsp;Joung-Liang Lan ,&nbsp;Ming-Shiou Jan ,&nbsp;Yu-Chao Chang ,&nbsp;Han Chang ,&nbsp;Chun-Hao Tsai ,&nbsp;Hui-Chen Chen ,&nbsp;Shin-Yi Liu ,&nbsp;Gregory J. Tsay","doi":"10.1016/j.clim.2025.110576","DOIUrl":"10.1016/j.clim.2025.110576","url":null,"abstract":"<div><div>Current serological markers for rheumatoid arthritis (RA) lack sensitivity in early or seronegative disease. We evaluated anti-BR1 antibodies, targeting a <em>Porphyromonas gingivalis</em> RgpA-derived peptide, as a novel biomarker. From 15 peptides screened in a training cohort, BR1 showed the highest diagnostic potential (AUC = 0.9553). In an independent validation cohort, anti-BR1 demonstrated an AUC of 0.7668, with 58.6 % sensitivity and 97.0 % specificity based on a ROC-derived cutoff. Anti-BR1 antibodies were detected in 82 of 140 (58.6 %) RA cases, including 35 of 58 (60.3 %) seronegative patients, and in 16 of 38 (42.1 %) early arthritis (EA) cases, outperforming RF and ACPA. Combining anti-BR1 with RF and ACPA increased the diagnostic yield from 58.6 % to 83.6 % in RA, and from 26.3 % to 55.3 % in EA.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110576"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144903087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial bioenergetic failure in SLE immunocytes: Targeting fitness for therapy","authors":"Anjali S. Yennemadi ,&nbsp;Natasha Jordan ,&nbsp;Sophie Diong ,&nbsp;Mark Little ,&nbsp;Joseph Keane ,&nbsp;Gina Leisching","doi":"10.1016/j.clim.2025.110571","DOIUrl":"10.1016/j.clim.2025.110571","url":null,"abstract":"<div><h3>Background</h3><div>Systemic Lupus Erythematosus (SLE) is characterized by dysregulated immune responses linked to immunometabolic perturbations. While mitochondrial dysfunction has been implicated in SLE, its cell-type-specific impact on immune subsets remains underexplored.</div></div><div><h3>Methods</h3><div>We repurposed existing RNA-seq data from SLE patient peripheral blood mononuclear cells, with a focus on nuclear-encoded mitochondrial (NEmt) genes, as well as mitochondrial genes themselves, to identify differentially expressed genes compared to healthy controls. Mitochondrial stress tests were performed on freshly isolated CD4+ T cells, CD8+ T cells, B cells, and monocytes from SLE patients and healthy donors to assess bioenergetic function.</div></div><div><h3>Results</h3><div>RNA-seq revealed that both NEmt genes and mitochondrial genes were downregulated in the PBMC population of SLE patients. In situ mitochondrial stress tests revealed significant reductions in oxygen consumption rate (OCR), indicating impaired oxidative phosphorylation (OXPHOS) across all immune subsets, while extracellular acidification rate (ECAR), a marker of glycolysis, remained unchanged. These findings highlight immune-cell-specific mitochondrial bioenergetic failure in SLE, without compensatory glycolytic adaptation.</div></div><div><h3>Conclusion</h3><div>Our results position mitochondrial fitness as a novel therapeutic target in SLE. We propose leveraging high-throughput screening of mitochondria-targeted compounds, including FDA-approved agents, to enhance OXPHOS, regulate mitophagy, or mitigate oxidative stress. This precision-based approach offers a paradigm shift from conventional immunosuppression to metabolic recalibration, with the potential to restore immune homeostasis in SLE.</div><div>Systemic Lupus Erythematosus (SLE) is characterized by dysregulated immune responses linked to immunometabolic perturbations. While mitochondrial dysfunction has been implicated in SLE, its cell-type-specific impact on immune subsets remains underexplored.Using existing RNA-seq data we focused on nuclear-encoded mitochondrial (NEmt) genes, as well as mitochondrial genes themselves. Mitochondrial stress tests were performed on freshly isolated CD4+ T cells, CD8+ T cells, B cells, and monocytes from SLE patients and healthy donors to assess bioenergetic function.RNA-seq revealed that both NEmt genes and mitochondrial genes were downregulated in the PBMC population of SLE patients. In situ mitochondrial stress tests revealed significant reductions in oxygen consumption rate, indicating impaired oxidative phosphorylation across all immune subsets, while glycolysis remained unchanged. These findings highlight immune-cell-specific bioenergetic failure in SLE and propose mitochondrial fitness as a novel therapeutic target in SLE. This precision-based approach offers a paradigm shift from conventional immunosuppression to metabolic recalibration.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"280 ","pages":"Article 110571"},"PeriodicalIF":4.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144686316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune profiling in solid organ transplant recipients with HHV-8 infection: Identification of immunological biomarkers for KICS and Kaposi's sarcoma","authors":"Rosalia Busà ,&nbsp;Francesca Timoneri ,&nbsp;Monica Miele ,&nbsp;Mariangela Di Bella ,&nbsp;Andrea Cona ,&nbsp;Salvatore Castelbuono ,&nbsp;Mattia Emanuela Ligotti ,&nbsp;Alessia Gallo ,&nbsp;Francesca Pecoraro ,&nbsp;Giuseppe Randazzo ,&nbsp;Caterina Amato ,&nbsp;Clara Pipia ,&nbsp;Giandomenico Amico ,&nbsp;Valentina Agnese ,&nbsp;Pier Giulio Conaldi ,&nbsp;Mario Luppi ,&nbsp;Alessandra Mularoni ,&nbsp;Matteo Bulati","doi":"10.1016/j.clim.2025.110562","DOIUrl":"10.1016/j.clim.2025.110562","url":null,"abstract":"<div><div>Human Herpesvirus 8 (HHV-8) poses a significant risk in solid organ transplant recipients (SOTRs). HHV-8 is implicated in both neoplastic and non-neoplastic conditions. This study investigates immune dysregulation in HHV-8-infected SOTRs by analysing cytokine profiles and virus-specific T cell responses across different clinical manifestations. Our findings reveal a progressive decline in HHV-8-specific T cell responses correlating with disease severity, alongside a distinct cytokine signature. KICS patients exhibit heightened inflammation with elevated IL-6, IL-10, IFNα, TNFα, IL-1β, IL-17 A, IDO, sCD14, and immune exhaustion markers (PD-1, LAG-3), whereas KS is associated with angiogenic and macrophage activation factors (HGF, CD163). Given these insights, monitoring HHV-8 DNAemia, inflammatory cytokines, and T cell functionality is crucial for early detection and risk stratification. This study underscores the importance of immune monitoring in transplant recipients, paving the way for targeted interventions to mitigate HHV-8-associated complications.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"280 ","pages":"Article 110562"},"PeriodicalIF":4.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144604458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Measuring efficacy for myasthenia gravis treatments: A review of biomarkers used in clinical trials","authors":"Taylor Wesley,&nbsp;Callie Rose,&nbsp;Jessica Ding,&nbsp;Kirstin Parkin","doi":"10.1016/j.clim.2025.110560","DOIUrl":"10.1016/j.clim.2025.110560","url":null,"abstract":"<div><div>Myasthenia gravis is an autoimmune disease that impairs neuromuscular transmission through autoantibodies, most commonly targeting acetylcholine receptors (AChR). While clinical scores like the Quantitative Myasthenia Gravis Score (QMGS) and the Myasthenia Gravis Activities of Daily Living Scale (MG-ADL) are commonly used in trials, there is no gold standard biomarker for evaluating treatment efficacy. This scoping review aimed to identify which biomarkers are most frequently used in randomized controlled trials (RCTs) for non-surgical treatments of generalized myasthenia gravis. We searched five databases for English-language RCTs published before May 9, 2024. Of 6685 screened texts, 33 met inclusion criteria. A total of 33 distinct biomarkers were tracked across studies, with AChR antibodies, IgG, and IL-2 most frequently reported. Biomarkers were measured inconsistently and at varied intervals, limiting cross-study comparability. The lack of standardized biomarker use hinders the ability to assess treatment efficacy and perform meta-analyses. We recommend developing consensus guidelines to improve future trial quality.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"280 ","pages":"Article 110560"},"PeriodicalIF":4.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}