Could be a crucial virulence factor for intracellular survival of M.tuberculosis (PubMed:23300718). Favors development of Th2-type response, and down-regulates the pro-inflammatory and Th1-type response (PubMed:19880448, PubMed:21451109). Specifically interacts with the human Toll-like receptor 2 (TLR2), leading to an early and sustained activation of p38 MAPK, which induces IL-10 production and activates Th2-type immune response (PubMed:19880448). Also inhibits pro-inflammatory cytokines IL-12p40 and TNF-alpha production. Acts by up-regulating the expression as well as tyrosine phosphorylation of suppressor of cytokine signaling 3 (SOCS-3), leading to the inhibition of phosphorylation of I-kappa-B-alpha, thereby preventing nuclear translocation of the NF-kappa-B/REL subunits and expression of NF-kappa-B regulated genes like IL-12 and TNF-alpha. Induction of SOCS-3 probably depends on the activation of p38 MAPK (PubMed:21451109). Interacts with human TLR2. Expression is positively regulated by Rv0485. The N-terminal region is responsible for interaction with TLR2 (PubMed:19880448). It is also important in mediating tyrosine phosphorylation of SOCS-3 (PubMed:21451109). Mice infected with the ppe18 deleted strain have reduced infection burden in lung, liver and spleen and have better survival rates compared to mice infected with the wild-type train. Belongs to the mycobacterial PPE family.