IL1B and neoplasm: Studies have shown that symbiotic bacteria activate MYD88 in myeloid cells, leading to the secretion of IL-23 and IL-1β, stimulating γδ T cells to produce IL-17, triggering local inflammation, and promoting the progression of lung cancer.[20] In pancreatic adenocarcinoma, microbes binding to TLRs on monocytes transform them into tumor-associated macrophages (TAMs), increase myeloid-derived suppressor cells (MDSCs), and inhibit the differentiation of CD4 T cells into Th1 cells, forming a suppressive tumor microenvironment.[13]