Yunping Cai , Jingjing Dou , Nihong Zhou , Han Shao , Xian Shen , Cui Lu , Xiaoli Fan , Song Guo Zheng
{"title":"Ferroptosis in patients with rheumatoid arthritis","authors":"Yunping Cai , Jingjing Dou , Nihong Zhou , Han Shao , Xian Shen , Cui Lu , Xiaoli Fan , Song Guo Zheng","doi":"10.1016/j.clim.2025.110588","DOIUrl":"10.1016/j.clim.2025.110588","url":null,"abstract":"<div><h3>Background</h3><div>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and joint destruction. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has recently emerged as a potential contributor to RA pathogenesis.</div></div><div><h3>Methods</h3><div>A systematic literature review was conducted to explore the mechanisms of ferroptosis in RA, focusing on iron metabolism dysregulation, oxidative stress, and immune cell dysfunction. Databases including PubMed, Embase, and Web of Science were searched for relevant studies.</div></div><div><h3>Results</h3><div>RA patients exhibit paradoxical iron distribution, with systemic deficiency but synovial overload, promoting ferroptosis. Key findings include: (1) Iron accumulation and lipid peroxidation exacerbate synovial inflammation; (2) Ferroptosis differentially affects immune cells (M1/M2 macrophages, T cells) and fibroblast-like synoviocytes (FLS); (3) Antioxidant defenses (GPX4) are impaired in RA, while some disease-modifying drugs (leflunomide, sulfasalazine) may modulate ferroptosis.</div></div><div><h3>Conclusion</h3><div>Ferroptosis plays a critical role in RA progression by disrupting synovial homeostasis. Targeting ferroptosis pathways offers promising therapeutic potential, though further research is needed to clarify cell-specific effects and optimize interventions.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110588"},"PeriodicalIF":3.8,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144921605","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}
Dingxian He , Lei Jin , Shuangshuang Wang , Huahua Zhong , Hongxi Chen , Hongyu Zhou , Zhangyu Zou , Chongbo Zhao , Xiao Huan , Jie Song , Jianying Xi , Chong Yan , Sushan Luo
{"title":"Efgartigimod versus standard of care in new-Onset AChR subtype generalized myasthenia gravis: A prospective cohort study","authors":"Dingxian He , Lei Jin , Shuangshuang Wang , Huahua Zhong , Hongxi Chen , Hongyu Zhou , Zhangyu Zou , Chongbo Zhao , Xiao Huan , Jie Song , Jianying Xi , Chong Yan , 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":"2025-08-21","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}
Yung-Ju Yeh , Hsin-Yi Peng , Ting-Yin Xue , Wei-Jing Li , Po-Hao Huang , Kai-Jieh Yeo , Chien-Chung Huang , Jiunn-Horng Chen , Chung-Ming Huang , Der-Yuan Chen , Joung-Liang Lan , Ming-Shiou Jan , Yu-Chao Chang , Han Chang , Chun-Hao Tsai , Hui-Chen Chen , Shin-Yi Liu , Gregory J. Tsay
{"title":"“Identification of an antibody against a novel peptide from Porphyromonas gingivalis as a biomarker for rheumatoid arthritis”","authors":"Yung-Ju Yeh , Hsin-Yi Peng , Ting-Yin Xue , Wei-Jing Li , Po-Hao Huang , Kai-Jieh Yeo , Chien-Chung Huang , Jiunn-Horng Chen , Chung-Ming Huang , Der-Yuan Chen , Joung-Liang Lan , Ming-Shiou Jan , Yu-Chao Chang , Han Chang , Chun-Hao Tsai , Hui-Chen Chen , Shin-Yi Liu , 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":"2025-08-21","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}
Lian Gui , Zena Chen , Liudan Tu , Liuzhong Zhou , Qiujing Wei , Jieruo Gu
{"title":"CD14+CD11c+HLA-II− monocytes are identified to be associated with osteoclastogenesis in ankylosing spondylitis","authors":"Lian Gui , Zena Chen , Liudan Tu , Liuzhong Zhou , Qiujing Wei , Jieruo Gu","doi":"10.1016/j.clim.2025.110586","DOIUrl":"10.1016/j.clim.2025.110586","url":null,"abstract":"<div><div>Abnormal monocytes are involved in the pathogenesis of ankylosing spondylitis (AS). We investigated the association between an imbalance of monocyte subpopulations and bone destruction in AS. Compared to controls, AS patients exhibited increased CD14<sup>+</sup>CD11c<sup>+</sup>HLA-II<sup>−</sup> monocytes and decreased CD14<sup>+</sup>CD11c<sup>+</sup>HLA-II<sup>+</sup> monocytes in peripheral blood. LPS stimulation promoted a shift from CD14<sup>+</sup>CD11c<sup>+</sup>HLA-II<sup>−</sup> monocytes toward CD14<sup>+</sup>CD11c<sup>+</sup>HLA-II<sup>+</sup> monocytes, enhancing the former's capacity to promote CD4<sup>+</sup> T cell proliferation. Micro RNA-seq analysis indicated that AS CD14<sup>+</sup>CD11c<sup>+</sup>HLA-II<sup>−</sup> monocytes were involved in osteoclast differentiation and overproduced soluble osteoclastogenic cytokine CSF-1. In 40 AS patients, evaluated CD14<sup>+</sup>CD11c<sup>+</sup>HLA-II<sup>−</sup> monocytes correlated positively with Spondyloarthritis Research Consortium of Canada (SPARCC) MRI inflammation score (<em>r</em> = 0.336, <em>P</em> = 0.034) and bone erosion score (<em>r</em> = 0.423, <em>P</em> = 0.007), but inversely with ankylosis score (<em>r</em> = −0.346, <em>P</em> = 0.029). Conversely, CD14<sup>+</sup>CD11c<sup>+</sup>HLA-II<sup>+</sup> monocytes showed the opposite correlation. Our findings demonstrate that expansion of CD14<sup>+</sup>CD11c<sup>+</sup>HLA-II<sup>−</sup> monocytes contribute to bone erosion in AS, potentially mediated through CSF-1-driven osteoclast differentiation.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110586"},"PeriodicalIF":3.8,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144879551","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}
Shuang Pan , Mengshu Yu , Bowei Fan , Bin Wang , Xinrui Yang , Jiawen Zhang , Xiaoqi Liu , Xiaojian Hong , Wei Yang
{"title":"Hydrogen protects against autoimmune myocarditis by inhibiting necroptosis via the TNF/TNFR1 signalling pathway","authors":"Shuang Pan , Mengshu Yu , Bowei Fan , Bin Wang , Xinrui Yang , Jiawen Zhang , Xiaoqi Liu , Xiaojian Hong , Wei Yang","doi":"10.1016/j.clim.2025.110577","DOIUrl":"10.1016/j.clim.2025.110577","url":null,"abstract":"<div><div>Autoimmune myocarditis refers to the inflammation of myocardial tissue caused by innate and adaptive immune responses, characterized by elevated levels of tumour necrosis factor-α (TNF-α), a classic pro-inflammatory factor. Although hydrogen exhibits anti-inflammatory and antioxidant properties, its therapeutic effects in autoimmune myocarditis have not been evaluated. Therefore, the present study aimed to explore whether hydrogen can alleviate autoimmune myocarditis via TNF-α. An experimental autoimmune myocarditis (EAM) model was established in BALB/c mice via subcutaneous injection of pig-derived myocardial myoglobin emulsified with complete Freund's adjuvant. The treatment group received 2 % hydrogen inhalation twice a day (3 h each time) for 21 days. CD4+ T cell expression was higher in the EAM group than in the Control group, and this increase was attenuated following treatment with hydrogen. Additionally, the levels of TNF-α and related inflammatory factors were substantially higher in the EAM group than in the Control group, and these changes were reversed following hydrogen treatment. Echocardiography assessments demonstrated a significant improvement in heart function following treatment with hydrogen compared to that in the EAM group. Pathological results revealed significant inflammatory cell infiltration and fibrosis in the hearts of the untreated EAM group. Tissue immunofluorescence and protein immunoblotting indicated elevated necroptosis markers in the EAM group, which were downregulated after treatment with hydrogen. This study demonstrates that hydrogen effectively ameliorated autoimmune myocarditis by modulating necroptosis via the TNF/TNFR1 signalling pathway, making it a promising novel therapeutic strategy for myocarditis.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110577"},"PeriodicalIF":3.8,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144830395","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}
Cheng Gong , Changming Zhang , Xu Han , Ying Jin , Yangyang Zhang , Chenlu Liu , Qintao Wang , Jiahui Zhang , Cheng Guo , Qing Zhou , Xiaomin Yu , Zhihong Liu
{"title":"Novel pathogenic MAN2B2 variants cause systemic lupus erythematosus and dysregulated glycosylation","authors":"Cheng Gong , Changming Zhang , Xu Han , Ying Jin , Yangyang Zhang , Chenlu Liu , Qintao Wang , Jiahui Zhang , Cheng Guo , Qing Zhou , Xiaomin Yu , 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":"2025-08-12","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}
Xing-Li Zhang , Meng-Meng Pan , Yaroslav Kaminskiy , Shi-Wei Jin , Jian-Qing Mi , Wei-Ping Zhang , Jie Xu
{"title":"Interleukin-5 is an adjunctive biomarker for engraftment syndrome in multiple myeloma patients undergoing autologous hematopoietic stem cell transplantation","authors":"Xing-Li Zhang , Meng-Meng Pan , Yaroslav Kaminskiy , Shi-Wei Jin , Jian-Qing Mi , Wei-Ping Zhang , Jie Xu","doi":"10.1016/j.clim.2025.110575","DOIUrl":"10.1016/j.clim.2025.110575","url":null,"abstract":"<div><div>Autologous hematopoietic stem cell transplantation (ASCT) in multiple myeloma (MM) can cause engraftment syndrome (ES), a clinical diagnosis without specific laboratory biomarkers. Herein, six cytokines commonly elevated during transplantation were chronologically detected during ASCT in 96 patients with newly diagnosed MM, 24.0 % of whom experienced ES. Among the molecules demonstrating remarkable peak levels, only IL-5 was able to differentiate ES from non-ES. IL-5 measured on day 12 emerged as an optimal indicator of ES, and its diagnostic value was enhanced when combined with the proportion of endogenous CD8<sup>+</sup> T cells after engraftment and daratumumab-naive history. Notably, IL-5 levels on day 6 (IL-5 D6) served as the earliest predictor. 70.8 % of the patients could be predicted as having ES or non-ES via the IL-5 D6 cutoff value and daratumumab treatment history. It suggests that IL-5 can aid in estimating ES, and prior exposure to daratumumab may reduce the incidence of ES.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"279 ","pages":"Article 110575"},"PeriodicalIF":3.8,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774794","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}
Guhan Luo , Rong Ni , Xuanwei Huang , Yuanhui Li , Dingcun Luo
{"title":"The role of signaling lymphocytic activation molecule (SLAM) family receptors in health and disease progression: Focusing on cancer and therapy","authors":"Guhan Luo , Rong Ni , Xuanwei Huang , Yuanhui Li , Dingcun Luo","doi":"10.1016/j.clim.2025.110574","DOIUrl":"10.1016/j.clim.2025.110574","url":null,"abstract":"<div><div>The SLAM family receptors are immunoglobulin superfamily receptors integral to immune cell communication and regulation. This review consolidates current knowledge on the structures and functions of SLAM family receptors members (SLAMF1–SLAMF9), emphasizing their roles within the tumor microenvironment. Notably, SLAMF7 has been extensively studied in multiple myeloma, serving as both a diagnostic marker and therapeutic target. Other SLAM family receptors are implicated in tumor immune evasion, drug resistance, and T-cell exhaustion. Emerging therapies, including monoclonal antibodies and combinations with immune checkpoint inhibitors, are evaluated. Despite promising findings, challenges such as functional redundancy and an incomplete understanding of the roles of SLAM family receptors across different cancer types persist. Ongoing research into their molecular mechanisms and clinical applications is essential for advancing effective cancer immunotherapies.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"280 ","pages":"Article 110574"},"PeriodicalIF":3.8,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144723368","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}
Junhan Wu , Zhe He , Weitao Zhuang , Xin Xia , Zijie Li , Aotian Mo , Yizhang Chen , Rixin Chen , Guibin Qiao
{"title":"Mechanisms of inflammation-driven lung cancer: From external influences to internal regulation","authors":"Junhan Wu , Zhe He , Weitao Zhuang , Xin Xia , Zijie Li , Aotian Mo , Yizhang Chen , Rixin Chen , Guibin Qiao","doi":"10.1016/j.clim.2025.110572","DOIUrl":"10.1016/j.clim.2025.110572","url":null,"abstract":"<div><div>Chronic inflammation is a crucial factor in the development and progression of lung cancer. External factors, such as indoor and outdoor air pollution and occupational hazards, along with imbalances in the lung microbiome, create a pro-inflammatory environment conducive to tumorigenesis. This review explores how various mechanisms drive the production of pro-inflammatory cytokines and immune modulators, leading to a tumor-promoting microenvironment. It also examines the roles of key cells in these processes and highlights the importance of epigenetic modifications in inflammation-driven lung cancer. Understanding these interactions provides insights into targeted therapeutic strategies and underscores the significance of addressing inflammation to reduce lung cancer risk.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"279 ","pages":"Article 110572"},"PeriodicalIF":3.8,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717678","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":"A specific bone marrow cytokine pattern in de novo acute myeloid leukemia","authors":"Noémie Ravalet , Hélène Guermouche , Pierre Hirsch , Frédéric Picou , Vincent Flament , Caroline Deswarte , Amélie Foucault , Jenny Beaud , Emmanuelle Rault , Emeline Saindoy , Sébastien Lachot , Mara Memoli , Nawa Hachem , Jean-Alain Martignoles , Valérie Gissot , Ludovic Suner , Emmanuel Gyan , Ollivier Legrand , Olivier Hérault , François Delhommeau","doi":"10.1016/j.clim.2025.110573","DOIUrl":"10.1016/j.clim.2025.110573","url":null,"abstract":"<div><div>Acute myeloid leukemia (AML) is a heterogeneous group of hematopoietic cancers. Cytokines play an important role in the regulation of normal and pathologic hematopoiesis. A pro-inflammatory state, described in hematopoietic malignancies, may participate in clonal selection. To identify recurrent cytokine patterns according to AML ontogenic subtypes, we quantified the concentration of 49 cytokines in the bone marrow (BM) plasma from 124 patients with AML or myelodysplastic syndrome (MDS), and from 94 healthy volunteers. We confirmed a pro-inflammatory profile in MDS and AML, with increased concentrations of CXCL8, CXCL10 and IL-6. Only a few cytokines varied when comparing AML to MDS. <em>De novo</em> AML subtypes carry a specific cytokine pattern dominated by the increase in CLEC11A concentrations and the decrease in FLT3 ligand concentrations. These cytokines could participate in clonal selection in this subtype of AML while being less critical in the other AMLs - <em>i.e.</em> secondary-like or <em>TP53-</em>mutated subtypes.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"280 ","pages":"Article 110573"},"PeriodicalIF":4.5,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144712889","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}