Journal of inflammation research · 2025
Single-Cell Transcriptomics Reveals CCL3+ Classical Monocyte Subset Linked to Autoimmune Pathogenesis.
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Xu Heng, Yuan Kai, Chen Guangyao, Luo Jing, Yan Aimin, Huang Huaijuan, Yu Xinbo, Tao Qingwen, Huang Guangrui, Xu Anlong
Аннотация
OBJECTIVE: The diverse differentiation states of mononuclear macrophages are closely associated with the pathogenesis of autoimmune diseases. This study integrates single-cell RNA sequencing data from six autoimmune diseases to characterize shared and disease-specific alterations in mononuclear macrophages, with the aim of enhancing our understanding of the immune landscape in autoimmune diseases and refining clinical treatment strategies.
METHODS: We collected single-cell RNA-sequencing data of autoimmune diseases including primary Sjogren's syndrome (pSS), Behçet's disease (BD), juvenile dermatomyositis (JDM), rheumatoid arthritis (RA), relapsing-remitting multiple sclerosis (RRMS), and systemic lupus erythematosus (SLE). We performed scRNA-seq analysis on 350,043 peripheral blood immune cells from autoimmune diseases patients and healthy controls, followed by validations with flow cytometry, immunohistochemical staining, and immunofluorescence.
RESULTS: Fifteen mononuclear phagocyte subpopulations were clustered from peripheral blood mononuclear cells (PBMCs), we identified a new subpopulation named CCL3+ classical monocytes (cMo) that is co-amplified in multiple autoimmune diseases (BD, JDM, pSS, RRMS, SLE). The CCL3+ cMo cells are characterized by high M1-like score, exhibiting strong inflammatory characteristics and high chemotaxis toward other monocytes. In addition, CCL3+ cMo cells upregulated antigen presentation-related signaling pathways, and the cytotoxic CD8+ T or memory CD8+ T cells were strongly perturbed by their signaling crosstalk.
CONCLUSION: This study delineates a comprehensive landscape of mononuclear phagocyte heterogeneity in autoimmune diseases and reveals CCL3+ cMo as a commonly amplified immune subset associated with multiple autoimmune diseases. These findings highlight its potential role in disease mechanisms and nominate CCL3+ cMo as a candidate therapeutic target.
METHODS: We collected single-cell RNA-sequencing data of autoimmune diseases including primary Sjogren's syndrome (pSS), Behçet's disease (BD), juvenile dermatomyositis (JDM), rheumatoid arthritis (RA), relapsing-remitting multiple sclerosis (RRMS), and systemic lupus erythematosus (SLE). We performed scRNA-seq analysis on 350,043 peripheral blood immune cells from autoimmune diseases patients and healthy controls, followed by validations with flow cytometry, immunohistochemical staining, and immunofluorescence.
RESULTS: Fifteen mononuclear phagocyte subpopulations were clustered from peripheral blood mononuclear cells (PBMCs), we identified a new subpopulation named CCL3+ classical monocytes (cMo) that is co-amplified in multiple autoimmune diseases (BD, JDM, pSS, RRMS, SLE). The CCL3+ cMo cells are characterized by high M1-like score, exhibiting strong inflammatory characteristics and high chemotaxis toward other monocytes. In addition, CCL3+ cMo cells upregulated antigen presentation-related signaling pathways, and the cytotoxic CD8+ T or memory CD8+ T cells were strongly perturbed by their signaling crosstalk.
CONCLUSION: This study delineates a comprehensive landscape of mononuclear phagocyte heterogeneity in autoimmune diseases and reveals CCL3+ cMo as a commonly amplified immune subset associated with multiple autoimmune diseases. These findings highlight its potential role in disease mechanisms and nominate CCL3+ cMo as a candidate therapeutic target.