Regulation of T Helper 17 by Bacteria: An Approach for the Treatment of Hepatocellular Carcinoma
A simplified diagram showing the possible mechanisms of intestinal bacteria in influencing the polarization of TH17 cells in the lamina propria. Activation of dendritic cells by intestinal microbes results in secretion of proinflammatory cytokines such as IL-12, L-23, IL-27. TH17-inducing bacteria may promote TH17 immunity via IL-23 induction, which may involve signaling mediated by the TLR ligands (a), extracellular ATP (b), and SAA (c). Meanwhile, some probiotic strains may skew immunity away from TH17 via IL-12 and IL-27 induction as a result of activating TLR and dectin receptors (a′). These cytokines can inhibit TH17 development while facilitate TH1 differentiation. Probiotic may also work by controlling the growth and colonization of TH17-inducing bacteria (d). IL: interleukin; P2X: ionotropic receptors; P2Y: metabotropic receptors; PAMPs: pathogen-associated molecular patterns; SAA: serum amyloid A; TLR: toll-like receptor.