Journal of Immunology Research最新文献

{"title":"Analysis of the Mediating Effect of Vitamin D via the TGF-β1/Treg Pathway in the Pathogenesis of Childhood Primary Immune Thrombocytopenia.","authors":"Peiling Li, Mengru Chen, Zhihang Wang, Rui Fan, Jia Guo, Bao Liu, Zhiyin Wang, Yanyan Ma, Dongju Zhao, Shujun Li","doi":"10.1155/jimr/4001873","DOIUrl":"10.1155/jimr/4001873","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the role of vitamin D (VitD), transforming growth factor-β1 (TGF-β1), and regulatory T cells (Treg) in the pathogenesis of primary immune thrombocytopenia (ITP) in children.</p><p><strong>Methods: </strong>From February 2023 to September 2024, 51 children with ITP and 44 healthy children from the First Affiliated Hospital of Xinxiang Medical College were enrolled. The serum levels of VitD and TGF-β1 and the percentage of Treg cells in peripheral blood were measured.</p><p><strong>Results: </strong>There was no significant difference in age and sex between the two groups (p  > 0.05). ITP group VitD, TGF-β1, and the level of Treg cells were significantly lower than those of the control group (p  < 0.05). In the ITP group, VitD and TGF-β1 (r = 0.421), Treg cells (r = 0.516), TGF-β1 and Treg cells (r = 0.563), and platelet count (r = 0.399, 0.305, 0.361, respectively, p  < 0.05). The median model analysis showed that VitD had a significant negative overall effect on ITP risk (regression coefficient = -0.014, p = 0.004), but its direct effect was no longer significant after the introduction of TGF-β1 and Treg, suggesting a complete mediation effect, where the path of VitD affecting ITP via TGF-β1 is significant (effect value = -0.015, p  < 0.001), but the mediated pathway involving Treg was not statistically significant.</p><p><strong>Conclusion: </strong>There is dysregulation of VitD, TGF-β1, and Treg cells in newly diagnosed children with ITP. TGF-β1 may be a key mediator of the regulation of ITP by VitD, suggesting the potential value of TGF- β1 as an intervening target.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e4001873"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crohn's Disease Phenotype in a Patient With Severe Congenital Neutropenia Caused by CSF3R Variants: Exploring the Pathogenesis and Effects of Thalidomide Treatment.","authors":"Yanqiu Wang, Lin Wang, Chun Pan, Zhiheng Huang, Ping Li, Xiaoxia Qiu, Cuifang Zheng, Ying Huang","doi":"10.1155/jimr/8163275","DOIUrl":"10.1155/jimr/8163275","url":null,"abstract":"<p><p>This study describes a case of severe congenital neutropenia (SCN) harboring biallelic CSF3R variants and presenting with a novel inflammatory bowel disease (IBD) phenotype that responded remarkably to thalidomide. We performed functional studies to reveal the pathogenicity of the CSF3R and to elucidate the potential mechanisms underlying the therapeutic effects of thalidomide. A comprehensive review of the literature identified 18 reported cases of SCN associated with CSF3R variants. We subsequently validated the pathogenicity of the variants in the patient's peripheral blood by flow cytometry, which demonstrated reduced granulocyte colony-stimulating factor (G-CSF) receptor (G-CSFR) expression and markedly decreased phosphorylation of signal transducer and activator of transcription (STAT)3 (p-STAT3) following stimulation with recombinant human G-CSF (rhG-CSF). Thalidomide augmented rhG-CSF-induced STAT3 phosphorylation in HEK293T cells harboring the CSF3R Q257  ^∗ or R308G/Q257  ^∗ variants, and this effect was suppressed by a Janus kinase (JAK)1 inhibitor. Thus, IBD might represent a novel phenotype of SCN caused by CSF3R variants, and thalidomide could potentially alleviate the symptoms by modulating the JAK1/STAT3 signaling pathway.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e8163275"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148549425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Auricularia auricula's Polysaccharides Confer Protection in Murine Sepsis via Immune Modulation.","authors":"Jesse Pereira Machado Viana, Luisa Coutinho Coelho, Priscila M Mendes, André Alvares Marques Vale, Jeferson Noslen Casarin, Joicy Cortez de Sá Sousa, Paulo Vitor Soeiro Pereira, Maria Carolina B Di Medeiros Leal, Anamelia L Bocca, Márcia C G Maciel","doi":"10.1155/jimr/9938963","DOIUrl":"10.1155/jimr/9938963","url":null,"abstract":"<p><p>Sepsis is a life-threatening condition characterized by severe organ dysfunction resulting from an uncontrolled host response to infection. Sepsis treatment poses a challenge due to its complexity and the need for effective therapeutic approaches. The objective of this study was to evaluate the immunomodulatory and antimicrobial effects of exopolysaccharides (EPS) from Auricularia auricula in a murine model of lethal sepsis. Our findings demonstrated that treatment with EPS significantly enhances the proliferation of circulating lymphocytes and granulocytes, which is associated with improved host defense mechanisms. Additionally, EPS administration effectively mitigates sepsis-induced pulmonary damage, as evidenced by preserved lung function. Furthermore, EPS treatment significantly reduces microbial translocation to the bloodstream, maintaining a lower colony-forming unit (CFU) count and thereby restricting systemic infection. The polysaccharides also prevent the development of thrombocytopenia in septic animals, thereby preserving platelet homeostasis. The compound modulates serum cytokine profiles, contributing to a more regulated inflammatory response. The interactome analysis reveals that the Dectin-1 → Syk pathway activates NF-κB/AP-1 and involves p38 MAPK, thereby explaining the observed cytokine modulation. The presence of Nod2/Ripk2 suggests that the EPS primes leukocytes to effectively combat both fungi and bacteria, leading to a reduced bacterial load and increased survival. Collectively, these data indicate that EPS, a prebiotic agent, represents a novel therapeutic strategy with potential for modulating immune responses, controlling microbial proliferation, and improving survival outcomes in a model of severe sepsis.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e9938963"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13507711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating Cell-Free RNA Reflects Immune-Associated and Airway Remodeling Signatures in Equine Asthma.","authors":"Birong Zhang, Hanna Agdour, Miia Riihimäki, Sanni Hansen, Amanda Raine","doi":"10.1155/jimr/5310284","DOIUrl":"10.1155/jimr/5310284","url":null,"abstract":"<p><p>Circulating cell-free RNA (cfRNA) has emerged as a promising minimally invasive biomarker capable of capturing transcripts originating from multiple tissues and cell types, but its utility in chronic inflammatory airway diseases remains poorly understood. Equine asthma (EA), a naturally occurring respiratory disease that shares key clinical and immunopathological features with human asthma, provides a valuable comparative model for evaluating plasma cfRNA in this context. We performed transcriptomic profiling of plasma cfRNA from horses with EA and healthy controls and compared these findings with partially matched bronchoalveolar lavage (BAL) and whole-blood (WB) transcriptomes. Differential abundance analysis of plasma cfRNA identified increased abundance of the epithelial alarmin IL33, together with signatures associated with tissue remodeling, cellular stress responses, and immune alterations. Notably, cfRNA from EA horses exhibited reduced B-cell-associated and increased T-cell-associated transcript signatures, a pattern independently supported by differential abundance, co-expression network, and deconvolution analyses. In contrast, similar immune-associated signatures were not evident in the BAL and WB transcriptomes analyzed in this study. Cross-compartment comparisons further demonstrated that plasma cfRNA captured a molecular profile largely distinct from those identified in BAL and WB, while sharing only a small set of differentially abundant transcripts across compartments. Collectively, these findings indicate that plasma cfRNA captures molecular patterns associated with EA that differ from those observed in conventional transcriptomic sampling compartments. These results support the potential utility of plasma cfRNA as a minimally invasive source of biomarkers for characterizing airway disease-associated molecular and immune alterations in both veterinary and comparative asthma research.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e5310284"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13509420/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148818664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Linking CD38 Cell Surface Expression to the Unique Calcium Flux Properties in Human Peripheral B Lymphocytes Following anti-IgM and anti-IgG Stimulation.","authors":"Viktória Temesfői, Péter Kaltenecker, Anna Nörenberg, Tímea Serény-Litvai, Ambrus Kaposi, Emese Mezősi","doi":"10.1155/jimr/1377217","DOIUrl":"10.1155/jimr/1377217","url":null,"abstract":"<p><p>CD38 serves as a marker for defining subsets of immune cells; however, being an ectoenzyme, it also plays a crucial part in modulating immunometabolic homeostasis, has immense potential to influence the microenvironment of tissues, functions as a prognostic indicator, as well as a therapeutic target. Despite the extensive information on CD38 and the scale of efforts in developing and optimizing therapies targeting various B cell-related diseases, there is still ongoing fundamental research addressing its basic functions on healthy human B cells, which is well needed. Using an adapted methodology to measure and analyze intracellular Ca²⁺ concentration changes in B cells upon anti-Ig activation, this study describes the possible effect of CD38 cell surface expression on the rapid Ca²⁺ flux response of different B cell subsets from healthy individuals, aiming to better understand the role and influence of CD38 on B cell behavior. Circulating B cell subpopulations bearing IgM type BCRs showed marked differences in their Ca²⁺ flux characteristics according to their respective expression levels of CD38, with the CD38^high transitional cells being visibly different from their transitional and naïve CD38⁺ and CD38^- counterparts, and the unswitched CD38^- cells being clearly distinct based on their Ca²⁺ flux pattern from the CD38⁺ cells in the same compartment, in a setting where CD38 expression was the sole differentiating factor among the subpopulations. The CD38^- unswitched cells had the highest maximum Ca²⁺ concentration among the IgM-expressing populations achieved during anti-IgM stimulation. IgG⁺ class-switched memory cells were clustered uniformly by their activation patterns, showed strong responses to anti-IgG stimulation, with no significant correlations to CD38 expression levels. While our research could not fully separate the functional effects of CD38, this work revealed descriptive data concerning the differential kinetic Ca²⁺ responses of circulating B cells, categorized by their CD38 expression levels.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e1377217"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13520786/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic Reprogramming of T Cells by MSCs Rebalances Th17/Treg Axis to Attenuate Collagen-Induced Arthritis.","authors":"Xiaoping Wang, Jingjing He, Qun Wang, Xue Liu, Haoming Yuan, Lu Jin, Meng Ding, Lin Yang, Shaoxin Cui, Fei Chang, Tong Xin, Hongtao Jin, Min Shi, Yongzhou Song, Wensen Pan, Aijing Liu","doi":"10.1155/jimr/1862250","DOIUrl":"10.1155/jimr/1862250","url":null,"abstract":"<p><strong>Background: </strong>Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by dysregulated T cell responses and metabolic disturbances. Mesenchymal stromal cells (MSCs) have shown therapeutic promise, but their mechanisms, particularly concerning T cell metabolism, remain incompletely defined. This study investigated whether human umbilical cord-derived MSCs (hUC-MSCs) ameliorate collagen-induced arthritis (CIA) by modulating T cell metabolism and differentiation.</p><p><strong>Methods: </strong>CIA was induced in DBA/1 mice. Animals received PBS or hUC-MSCs on day 28. Arthritis index (AI), joint histology, serum cytokines (TNF-α, IL-6, IL-17, and TGF-β), and metabolites (lactate and pyruvate) were assessed. Splenic T cell transcription factors (FOXP3, RORγt, and PU.1) and glycolytic genes (GLUT1, G6PD, and PFKFB3) were analyzed by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot. In vitro, human CD4⁺ T cells were cocultured with hUC-MSCs under T-helper 17 (Th17)-polarizing conditions. T cell subsets, glycolytic metabolites, and gene/protein expression were evaluated by flow cytometry, colorimetric assays, RT-qPCR, and western blot.</p><p><strong>Results: </strong>MSC treatment significantly attenuated arthritis severity, joint destruction, and splenomegaly in CIA mice. It reduced serum pro-inflammatory cytokines and normalized elevated lactate and pyruvate levels. In the spleen, MSCs suppressed RORγt and PU.1 while enhancing FOXP3 expression, and downregulated GLUT1 and G6PD mRNA. Positive correlations were found between glycolytic markers (GLUT1 and G6PD) and pro-inflammatory transcription factors (RORγt and PU.1), and between serum lactate and inflammatory cytokines. In vitro, hUC-MSCs directly inhibited Th17 differentiation and promoted Treg generation in human CD4⁺ T cells. This metabolic reprogramming was functionally coupled to a shift in T cell differentiation: a suppression of pro-inflammatory Th17 cells and a promotion of regulatory T (Treg) generation in human CD4⁺ T cells. This was accompanied by reduced lactate production and significant downregulation of GLUT1, G6PD, and PFKFB3 at both mRNA and protein levels.</p><p><strong>Conclusions: </strong>hUC-MSCs ameliorate CIA by restoring the Th17/Treg balance through metabolic reprogramming of T cells, specifically by suppressing glycolysis. This immunometabolic mechanism highlights the therapeutic potential of MSCs in RA.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e1862250"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13247138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148205188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cytokine Signatures Outperform Immune Subsets in Machine Learning Models for Predicting Acute Graft-Versus-Host Disease at Neutrophil Engraftment.","authors":"Mohini Mendiratta, Praful Pandey, Shobhit Pandey, Sandeep Rai, Meenakshi Mendiratta, Hridayesh Prakash, Shuvadeep Ganguly, Archana Sasi, Ritu Gupta, Prabhat Singh Malik, Raja Pramanik, Sachin Kumar, Baibaswata Nayak, Riyaz Ahmed Mir, Sameer Bakhshi, Deepam Pushpam, Mukul Aggarwal, Aditya Kumar Gupta, Rishi Dhawan, Tulika Seth, Manoranjan Mahapatra, Ranjit Kumar Sahoo","doi":"10.1155/jimr/1066614","DOIUrl":"10.1155/jimr/1066614","url":null,"abstract":"<p><strong>Background: </strong>Acute graft-versus-host disease (aGvHD) is a major immune complication of allogeneic hematopoietic stem cell transplantation (Allo-HSCT), driven by complex immune-cytokine interactions. This study employed machine learning (ML) algorithms to develop early predictive models for aGvHD using immune and cytokine profiles of Allo-HSCT recipients at the time of engraftment.</p><p><strong>Materials and methods: </strong>Seventy patients with hematological disorders undergoing their first Allo-HSCT were recruited prospectively. Peripheral blood immune subsets and cytokines were analyzed using flow cytometry and ELISA, respectively. ML models, including support vector classifier (SVC), decision tree, and random forest, were trained on 48 features: 34 immune subsets and 14 cytokines.</p><p><strong>Results: </strong>Patients who developed aGvHD exhibited a reduced CD4⁺/CD8⁺ ratio, lower Tregs, elevated Th1, Th17, cytotoxic natural killer (NK) cells, dendritic cells (DCs), B cell, and increased proinflammatory cytokines (IFN-γ, IL-1β, IP-10, TNF-α, IL-17α, IL-12p70, MIP-1α, MIP-1β, and RANTES). ML models demonstrated excellent predictive performance, with cytokine profiles alone or combined with immune data achieving perfect accuracy (1.00), followed by T-cell (0.96), NK cell (0.93), DC (0.90), and B cell (0.86) models.</p><p><strong>Conclusion: </strong>Cytokine profiles emerged as superior predictors over immune subsets, supporting their integration into ML-based aGvHD risk prediction. These findings provide a foundation for developing biomarker-guided strategies for early aGvHD detection and management.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e1066614"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD47 Expression in Classic Hodgkin Lymphoma and Its Association With Tumor Microenvironment.","authors":"Xiaoyue Xiao, Lin Nong, Yiyang Luo, Jiyan Dong, Xujie Sun, Kang Jiang, Xuemin Xue, Xiaoli Feng","doi":"10.1155/jimr/1680256","DOIUrl":"10.1155/jimr/1680256","url":null,"abstract":"<p><p>Cluster of differentiation 47 (CD47) has been reported to overexpress in various malignant tumors and is associated with inferior prognosis. However, the critical role of CD47 in classic Hodgkin lymphoma (CHL) and its association with immune checkpoints and tumor microenvironment (TME) remain unclear. Tumor tissues of CHL from Cancer Hospital, Chinese Academy of Medical Sciences and the public dataset from GSE17920 were analyzed. Immunohistochemistry was performed to detect the expression of CD47, programmed cell death protein 1 (PD-1), and PD ligand 1 (PD-L1) in CHL. Kaplan-Meier curves and Cox model were used for comparing the clinical outcomes of patients belonging to different subgroups. Bioinformatic analyses included differentially expressed genes (DEGs) screening, functional enrichment, and immune infiltration (CIBERSORT) were performed using GSE17920. In the study, CD47 expression was analyzed in both tumor cells (CD47tumor_score) and the TME (CD47micro_score) of CHL patients. High CD47tumor_score was associated with poorer progression-free survival (PFS) (p = 0.04). Meanwhile, high CD47micro_score was significantly correlated with worse PFS (p = 0.02). Univariate Cox regression identified high CD47micro_score as a significant predictor of inferior overall survival (OS; hazard ratio [HR] = 4.91, p = 0.03). Additionally, high CD47 expression correlated with increased PD-L1, and patients with concurrent high CD47 and positive PD-L1 of tumor cells had the shortest PFS, although this trend was not statistically significant. Importantly, a synergistic prognostic effect between CD47 and PD-L1 was that patients with high CD47 and/or PD-L1 of immune cells had significantly worse PFS than those with low expression of both markers. Analysis of public data (GSE17920) confirmed that high CD47 mRNA expression was associated with worse PFS (p = 0.02). Functional enrichment analyses revealed that high CD47 expression was linked to pathways involving chemokine signaling and immune cell migration, with increased infiltration of M1 macrophages, neutrophils, and eosinophils in the TME. CD47 might be involved in the disease progression and prognosis of CHL, it had a closely positive correlation with PD-L1. Targeting of CD47 and PD1/PDL1 might provide a promising strategy in CHL.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e1680256"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CAR-Cell Therapy for Autoimmune Diseases: From the Laboratory to Clinical Practice.","authors":"Xiao-Peng Zhang, Yi-Dong Chen, Qi Yu, Fang Liu, Jia-Min Li, Shuang Li, Yi-Yu Cheng, Xiao-Yu Fu, Qian-Xi Xia, Jun-Rong Li, Xiao-Hua Hou, Liang-Ru Zhu","doi":"10.1155/jimr/6629562","DOIUrl":"10.1155/jimr/6629562","url":null,"abstract":"<p><p>Autoimmune diseases (AIDs) are characterized by a breakdown in immune tolerance, wherein the patient's immune system fails to recognize self-tissues and subsequently attacks the body's organs and tissues. Although there are many therapeutic medicines targeting the pathogenic mechanisms, there is currently a lack of curative or long-term symptom control options. Chimeric antigen receptor (CAR) cells are engineered cells that express multifunctional synthetic receptors. These CAR cells specifically target killer pathogenic immune cells and offer a novel approach to treating AIDs by modulating the immune microenvironment. Recent studies have demonstrated satisfactory outcomes with this method in managing autoimmune conditions. In our review paper, we provide a comprehensive summary of previous cases utilizing CAR cell therapy for AIDs. We hope that our review will provide clinicians with more options for the treatment of AIDs.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e6629562"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Abnormal Expression of B7-H4 Is Associated With the Pathogenesis of Autoimmune Thyroid Diseases.","authors":"Yuqing Wu, Jianbin Xu, TianTian Cai, Yudie Fang, Zhaowei Huang, Xinwei Zhang, Guangxin Li, Wenyu Xu, Jinan Zhang","doi":"10.1155/jimr/5529891","DOIUrl":"10.1155/jimr/5529891","url":null,"abstract":"<p><strong>Background: </strong>B7-H4 is an immunosuppressive molecule extensively studied in tumor diseases and is also of interest in some autoimmune diseases. However, the relationship between B7-H4 and autoimmune thyroid diseases (AITDs) has not been explored.</p><p><strong>Objective: </strong>To investigate the B7-H4 expression in different tissues of patients with different subtypes of AITDs.</p><p><strong>Methods: </strong>The B7-H4 protein expression in thyroid tissue of the participants was identified through immunohistochemical analyses while concentrations of plasma soluble B7-H4 (sB7-H4) were detected by enzyme-linked immunosorbent assay (ELISA). Additionally, B7-H4 mRNA expression in peripheral blood mononuclear cells (PBMCs) was evaluated via RT-PCR.</p><p><strong>Results: </strong>The immunohistochemical findings revealed a decrease in levels of B7-H4 protein in thyroid tissue of Graves' disease (GD) and Hashimoto's thyroiditis (HT) patients, compared with those of the normal controls. Similarly, a decrease was observed in the level of B7-H4mRNA expression in PBMCs assayed via RT-PCR. However, based on ELISA results, plasma levels of sB7-H4 were increased in both GD and HT patients compared to those in normal controls.</p><p><strong>Conclusion: </strong>The abnormal expression of B7-H4 in AITD patients suggests that it may be involved in the onset and progression of the disease. At the same time, the mechanism of action of B7-H4 in AITD and whether it is a potential therapeutic target need to be further studied.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e5529891"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}