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High expression of IRF8 in AChR-specific cells regulates the function of B cells
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DOI：10.1016/j.imlet.2026.107154.png)
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Abstract
En 中文
Myasthenia gravis (MG) is a kind of autoimmune disease. Interferon regulatory factor 8 (IRF8) is an interferon common sequence-binding protein. IRF8 is a key factor involved in the development, maturation, and antimicrobial activity of myeloid cells. Second-generation sequencing of splenocytes at the peak period of disease in experimental autoimmune MG (EAMG) rats and complete Freund's adjuvant (CFA)-treated mice suggested that the expression of IRF8 gene is related to the pathogenesis of EAMG. This study focused on the differential expression of IRF8 in B cell and T cell in EAMG, and the underlying mechanism of the role of IRF8 in the pathogenesis of the disease. We analyzed the gene expression profiles of splenocytes from CFA-treated and EAMG mice. We measured the serum anti-acetylcholine receptor autoantibody titer, IRF8 mRNA and protein level in splenocytes, IRF8 mRNA and protein expression in T and B cells as well as in LPS-stimulated splenocytes, and colocalization of CD45R and IRF8 proteins using confocal microscopy. Finally, we determined the titers of anti-acetylcholine receptor autoantibodies in the supernatants of LPS-stimulated cells. Our findings revealed that the expression of IRF8 in splenocytes increased during the peak period of EAMG, B cells exhibited high IRF8 expression, and that IRF8 expression in B cells was positively correlated with antibody secretion. Taken together, our findings indicate that IRF8 is a potential biomarker for EAMG diagnosis.
Keywords:
IRF8
Experimental autoimmune myasthenia gravis
T cell
B cell
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