B lymphocytes acquire myeloid and autoimmune phenotypes via the downregulation of lymphocyte-specific protein-1.

A recent preprint study explores the role of actin-binding proteins (ABPs) in B lymphocytes and their impact on immune responses. The study found that the ABP LSP1 is a key regulator of innate immune responses in B cells. LSP1 deficiency in B cells led to the upregulation of myeloid genes and the acquisition of myeloid morphology. Additionally, LSP1 deficiency resulted in dual functionality in B cells, exhibiting both strong phagocytic activity and high antibody production. The study also found that LSP1 deficiency induced the production of autoantibodies and accelerated the progression of experimental lupus in mice. The expression of LSP1 in B cells was downregulated in lupus patients and inversely correlated with myeloperoxidase expression. The findings highlight the critical involvement of LSP1 in promoting autoimmune responses and generating functionally chimeric B cells. [Extracted from the article]