Figure 2.

Origins and specificities of Treg during infections. The origin and antigen specificity of Treg may vary according to the site and the nature of the infection. In acute infection, tissue damage may be associated with enhanced presentation of self antigens. In this case, self-reactive natural Treg may be activated and could, in a bystander manner, limit effector responses against the pathogen. At sites of infection various populations of microbe-specific Treg can be induced (e.g. converted Foxp3⁺ Treg (cFoxp3⁺), Th1 cells producing IL-10 or inducible T reg (Tr1 cells)). In some chronic infections, there is evidence that natural Treg may also accumulate at sites of infection and can recognize microbial antigens. In an environment that is rich in TGF-β and the vitamin A metabolite retinoic acid (RA), such as the gut, peripheral conversion of Foxp3⁻ T cells into Foxp3⁺ Treg may occur in response to food or gut flora antigen or during oral infection. These converted Foxp3⁺ T cells could potentially limit immune responses. Some of these converted cells may be able to recirculate and could contribute to the control of peripheral homeostasis. Red arrows indicate control of immune responses.