Fig. 2

AIM2 regulatory network of multiple cell subpopulations in rheumatoid arthritis (RA). Aberrant expression of AIM2 in various cells in RA promotes different manifestations of RA, including bone destruction, angiogenesis, inflammation, and RA-associated atherosclerosis. For example, upregulation of AIM2 expression promotes excessive apoptosis in healthy T cells, and overexpression of TAK1 may inhibit PANoptosis in autoimmune T cells and FLS to promote self-survival. The BCL6/BLIMP1 axis regulates osteoclast and B cell differentiation via AIM2. The upregulation of AIM2 in FLS promotes cell proliferation and the subsequent release of inflammatory factors and bone destruction mediators. The upregulation of POP3 in monocytes suppresses AIM2 expression and promotes monocyte survival and differentiation into proinflammatory macrophages. The presence of AIM2 positive regulators (black) and AIM2 negative regulators (red) in macrophages affects macrophages and their downstream inflammatory processes through different mechanisms