Figure 1.

A possible mechanism for the maintenance of an infection-triggered immune regulatory environment. (A) Foreign, pathogen-derived antigens would activate and initially expand regulatory T cells (Treg) that crossreact with self-antigens and allergens, as well as pathogen-specific regulatory cells. (B) Self-antigens or common allergens would further expand and activate the crossreactive Treg cells. (C) Regulatory cell-derived IL-10 and TGF-β would inhibit potentially pathogenic immune responses by: (a) diverting the differentiation of naïve, Th0 lymphocytes to T regulatory lineages rather than to other, proinflammatory types (22, 23); (b) promoting the differentiation of tolerogenic antigen-presenting cells (APC) (these cells would lead to the differentiation of regulatory T and B lymphocytes) (24); (c) directly inhibiting the proliferation of and synthesis of proinflammatory cytokines by effector T cells (20, 21). Self- or allergen-reactive Th1 cells would sporadically release the IL-2 necessary to maintain the Treg response, before being controlled by regulatory cytokines. For the sake of clarity, the inflammatory reaction due to infection in (A), the APC required for Treg antigen recognition in (A,B), and regulatory B cells are not depicted in the Figure.