Skip to main content
. 2022 Sep 19;19(1):315–327. doi: 10.1007/s11302-022-09891-1

Fig. 1.

Fig. 1

The release of eATP from the gut microbiota can induce apoptosis of Tfh cells and regulate IgA release by binding to P2X7 receptors on Tfh cells in Peyer’s patches (PPs). Also, the intestinal commensal SFB can induce the differentiation of Th17 and Tfh and stimulate the release of IgA with other cytokines. When the intestinal environment is stable, IgA produced in PPs can play a protective role in the intestinal environment. In contrast, once the homeostasis of the intestinal environment gets disrupted, SFB induces a strong autoimmune response. Inosine (INO), which is metabolized by some microorganisms in the gut, can act as a purinergic signalling factor binding to A2AR on the surface of CD4+ T cells, inhibiting the differentiation of helper T cells to play a Treg-like role. However, in a tumor environment or the presence of other inflammatory factors infiltration, the inosine-A2AR axis can play the opposite role and promote T cell differentiation