SH3BP2 Deficiency Ameliorates Murine Systemic Lupus Erythematosus

Background: The adaptor protein Src homology 3 domain-binding 2 (SH3BP2) is widely expressed in immune cells. It controls intracellular signaling pathways. present study was undertaken to investigate the role of SH3BP2 a murine systemic lupus erythematosus model. Methods: For model, we used Faslpr/lpr mice. Clinical and immunological phenotypes were compared between SH3BP2-deficient Splenomegaly renal involvement assessed. Lymphocyte subsets spleen analyzed by flow cytometry. To examine specific cells, B cell-specific mice analyzed; T cells bone marrow-derived dendritic macrophages vitro. Results: deficiency significantly reduced lupus-like phenotypes, presented as splenomegaly, involvement, elevated serum anti-dsDNA antibody, increased splenic B220+CD4−CD8− Notably, did not rescue phenotypes. Furthermore, substantially affect characteristics Interestingly, suppressed differentiation vitro number lupus-prone Conclusions: ameliorated manifestations. Modulating expression could thus provide novel therapeutic approach autoimmune diseases.