Fig. 3

The interplay between the adaptive immune system and the gut microbiota in GI tract. Some mechanisms utilized by the gut microbiota to interact with the host innate immune system in GI tract are described above. Foxp3 + Treg cells promote maturation of B cells and production of secretary IgA. These contribute to the regulation of homeostatic microbiota composition and the maintenance of a non-inflammatory host-microbial relationship. CD8 + T cells can be activated by the intestinal microbiota and its metabolites. Butyrate, for instance, showed a direct antagonistic influence on the HDAC of CTLs and Tc17 cells, thereby promoting the expression of IFN-γ and granzyme B. As for Th cells, the adhesion of SFB to IECs is a common outcome of inducing homeostatic intestinal Th17 cells. Tfh cells, being another modulation target of gut microbiota modification, are essential for the production of plasma cells and memory B cells. The SCFAs have been demonstrated to regulate the size and function of the Treg cell pool