CD4 and Sepsis: Previous studies have shown that in sepsis, CD4+ T cells bind to macrophages via MHC II to downregulate TLR‐induced proinflammatory signaling.[38] In tumors, macrophages promote the conversion of Th1 cells to Th2 cells and influence Treg cell proliferation, migration, and function through various mechanisms.[39, 40] In renal tissue, macrophages stimulate helper T cells to exacerbate kidney inflammation.[41] These studies highlight the crucial regulatory role of macrophages in the proliferation, activation, and function of helper T cells in several diseases.