Thus, infections that activate the toll-like receptor 2 (TLR2) in vivo (specifically through TLR1/2 heterodimers) could shift the ratio between the Treg and the HIV inhibitor T helper 17 (Th17) cells’ balance toward a pro-inflammatory state in multiple sclerosis, thereby promoting disease activity and progression [89]. Here, TLR2 is linked to multiple sclerosis.