Figure 1.

Mechanisms of immune homeostasis modulation: (a) During intrauterine life, the fetus represents an antigenic non-self for the maternal immune system. This outcome does not occur due to the fetus peculiar prevalence of Th-2-type immune responses. After birth, however, the Th2-polarized cytokine milieu is inadequate to counter some infections. (b) In the first months of life, the antigenic ‘pressure’ provided by a highly diversified, eubiotic microbial biomass would play a decisive role in training the immune system. (c) Principal players in immune homeostasis are regulatory T-lymphocytes (Treg), activated by dendritic cells through commensal components and metabolites acting as ligands of receptors such as Toll-like receptors (TLR1 and TLR2) and G- protein coupled receptors (GPR41, GPR43, GPR109), respectively. Th1 cells generate IFN-γ and are involved in cell-mediated immunity; Th2 cells produce IL-4 and contribute to humoral immunity; IL-17-producing Th17 cells play a strategic role in immune responses to extracellular pathogens and fungi. However, Th subset continuous overexpression is involved in autoimmune, inflammatory, and allergic diseases.