Journal of Immunology Research最新文献

{"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":3.6,"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":"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":3.6,"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 Impact of Monkeypox Virus Infection on Pregnancy Outcome: Clinical Features and Potential Pathogenic Mechanisms.","authors":"Jingyi Wu, Fangbin Huang, Qingliang Zheng","doi":"10.1155/jimr/5158686","DOIUrl":"10.1155/jimr/5158686","url":null,"abstract":"<p><p>Monkeypox has garnered significant attention following its emergence in multiple countries and its designation as a global health emergency in 2022. There is a notable deficiency in clinical and experimental data regarding pregnancy outcomes following monkeypox infection. The complications associated with monkeypox virus (MPXV) infection, including fetal miscarriage, preterm delivery, and congenital infections, have not been adequately addressed, and there is a lack of effective clinical interventions. Two clades of MPXV have been identified: clades I and II, with clade I being the predominant strain previously associated with adverse pregnancy outcomes. Clade IIb has also been implicated in potential vertical transmission from mother to child. Infection of a pregnant individual with MPXV can lead to fetal conditions, such as generalized diffuse herpes hydatidis and extensive hemorrhage within the placenta. MPXV is thought to evade the immune response primarily by inhibiting interferon (IFN)-mediated antiviral effects, suppressing host immune recognition, dampening host inflammatory responses, and modulating cellular apoptosis. This review aims to provide a comprehensive overview of the clinical manifestations, potential routes of vertical transmission, and possible pathogenic mechanisms of MPXV infection in pregnant women, thereby serving as a valuable reference for future diagnostic, therapeutic, and pharmacological strategies in managing MPXV-related pregnancy complications.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e5158686"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433339","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":3.6,"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":"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":3.6,"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}

{"title":"SARS-CoV-2-Induced Macrophage Polarization Reverses HIV-1 Latency in J-Lat Cells Through TNFα Signaling.","authors":"Patricio Jarmoluk, Franco Agustín Sviercz, Cintia Cevallos, Rosa Nicole Freiberger, Cynthia Alicia López, M Victoria Delpino, Jorge Quarleri","doi":"10.1155/jimr/9986845","DOIUrl":"10.1155/jimr/9986845","url":null,"abstract":"<p><strong>Introduction: </strong>Coronavirus disease 2019 (COVID-19) may have both short- and long-term impacts on the progression of human immunodeficiency virus (HIV)-1 after acute SARS-CoV-2 infection in people living with HIV (PLWH), even those on combined antiretroviral therapy (cART). This study aimed to investigate whether SARS-CoV-2 could influence HIV reactivation in latently infected lymphoid cells.</p><p><strong>Methods: </strong>HIV-infected lymphoid (J-Lat) cells, characterized by proviral latency under unstimulated conditions, were used for latency reversal assays with phorbol 12-myristate 13-acetate (PMA), free SARS-CoV-2 particles, or conditioned media (CM) from macrophages. Monocytes isolated from donor blood were differentiated into macrophages (monocyte-derived macrophages [MDMs]) and polarized to M1 or M2 phenotypes before stimulation or with two SARS-CoV-2 variants (wild-type and BA.5) infection. Additionally, the effects of redox imbalance on latency reversal in both J-Lat and myeloid (U1) latency models were measured. SARS-CoV-2 RNA was quantified by RT-qPCR targeting ORF1ab and N genes, and latency reversal and reactive oxygen species (ROS) levels were assessed by flow cytometry. TNFα involvement was confirmed through neutralization assays, while cytokines and polarization markers were analyzed via ELISA and fluorescent antibodies.</p><p><strong>Results: </strong>Jurkat and J-Lat cells had low ACE2 expression and were not permissive to SARS-CoV-2 infection. SARS-CoV-2 exposure alone did not induce HIV latency reversal in J-Lat cells. However, CM from M1-polarized, resiquimod (R-848)-treated, and SARS-CoV-2-infected macrophages significantly reactivated latent HIV. TNFα was identified as the primary driver of latency reversal, with no significant changes in ROS levels. Prolonged SARS-CoV-2 exposure shifted macrophage polarization toward an anti-inflammatory M2 phenotype, characterized by IL-10 release, which reduced latency reactivation.</p><p><strong>Conclusions: </strong>This study demonstrates that SARS-CoV-2 can indirectly reverse HIV latency in lymphoid cells by promoting the release of pro-inflammatory cytokines from infected macrophages. These findings suggest potential therapeutic strategies for preventing HIV reactivation during SARS-CoV-2 coinfection, emphasizing the modulation of cytokine signaling to control inflammation while minimizing immune dysregulation.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e9986845"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433417","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":"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":3.6,"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":"RETRACTION: Glycyrrhizin Attenuates Toll Like Receptor-2, -4 and Experimental Vasospasm in a Rat Model.","authors":"Journal Of Immunology Research","doi":"10.1155/jimr/9817675","DOIUrl":"10.1155/jimr/9817675","url":null,"abstract":"","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e9817675"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433426","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 Role of IFN-γ-Mediated Immune Cell Crosstalk in the Pathogenesis of Aplastic Anemia.","authors":"Shuai Tan, Yumeng Li, Yaochi Chen, Wanling Sun","doi":"10.1155/jimr/2216487","DOIUrl":"10.1155/jimr/2216487","url":null,"abstract":"<p><p>Interferon-gamma (IFN-γ) is a central mediator of immune-driven bone marrow failure (BMF) in acquired aplastic anemia (AA). Persistent IFN-γ signaling alters the bone marrow microenvironment by activating the JAK-STAT1 pathway, which results in immunological imbalance, inflammatory amplification, and depletion of hematopoietic stem and progenitor cells (HSPCs). IFN-γ disturbs HSPC quiescence and self-renewal, interferes with thrombopoietin (TPO)-c-Mpl communication, and stimulates cytotoxic T-cell-dominant immunological responses. Simultaneously, IFN-γ destabilizes local immunological homeostasis by disrupting immune crosstalk through the IDO1 axis and regulatory T-cell (Treg) malfunction. In addition to discussing new therapeutic methods, such as Treg-based therapies and JAK inhibition, as prospective precision approaches for AA, this review incorporates current mechanistic insights into IFN-γ-driven cellular interactions inside the bone marrow niche.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e2216487"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433397","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":"Lnc-CHRM4-2:1 Inhibits M2 Polarization and Efferocytosis of Macrophages by Downregulating MerTK and SLC2A1 in Rheumatoid Arthritis.","authors":"Jinjin Chu, Jie Zang, Lili Zhang, Zhuojian Qu, Haibo Li, Chunjuan Yang, Jiamei Sun, Linlin Gai, Xuecheng Sun, Donghua Xu","doi":"10.1155/jimr/1718207","DOIUrl":"10.1155/jimr/1718207","url":null,"abstract":"<p><strong>Objective: </strong>Rheumatoid arthritis (RA) is a common chronic and systemic autoimmune disease. Long noncoding RNAs (lncRNAs) have been documented to play important roles in the pathogenesis of RA. This study is aimed to investigate the differentially expressed lncRNAs in RA and explore the underlying roles and mechanisms of RA-specific lncRNAs.</p><p><strong>Methods: </strong>Peripheral blood mononuclear cells (PBMCs) from three RA patients and three healthy controls were detected by transcriptome sequencing analysis. Enrichment analysis was performed to identify the potential functional categories and signal pathways. The expressions of the screened dysregulated lncRNAs in RA were further validated using quantitative real-time polymerase chain reaction (qRT-PCR). The effects of the candidate lncRNA lnc-CHRM4-2:1 on the proliferation and apoptosis of Raw264.7 cells were determined by cell counting kit-8 (CCK-8), 5-ethynyl-2'-deoxyuridine (EdU) proliferation assays, and Annexin V-APC/PI staining flow cytometry assay. qRT-PCR and western blot were performed to detect the expression of functional molecules related to M1/M2 macrophage polarization and efferocytosis.</p><p><strong>Results: </strong>The expression of lnc-CHRM4-2:1 was significantly higher in PBMCs of RA patients compared to healthy controls. Lnc-CHRM4-2:1 was negatively associated with the level of serum CCP of RA patients, suggesting that it was a RA-specific lncRNA. Overexpression of lnc-CHRM4-2:1 could potentially affect cell proliferation and apoptosis, promote M1 polarization, inhibit M2 polarization, and the mRNA and protein expressions of MerTK and SLC2A1 in Raw264.7 cells.</p><p><strong>Conclusion: </strong>Lnc-CHRM4-2:1 is an RA-specific lncRNA, which inhibits macrophage M2 polarization and efferocytosis by downregulating MerTK and SLC2A1. Lnc-CHRM4-2:1 may be considered a potential diagnostic biomarker and therapeutic target for RA.</p>","PeriodicalId":15952,"journal":{"name":"Journal of Immunology Research","volume":"2026 1","pages":"e1718207"},"PeriodicalIF":3.6,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13140872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433311","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}