CD4’T cells play a key role in regulating immune system function. When these regulatory processes go awry, organ-specific autoimmune diseases may develop. Here, Roland Liblau, Steven Singer and Hugh McDevitt explore the thesis that a particular subset of 04’ T cells, namely 7 helper 1 (Tbl) cells, contributes to the patbogenesis of organ-specific autoimmune diseases, while another subset, Tb2 cells, prevents them.

It is now clear that the T helper (Th)-cell population comprises functionally distinct subsets that are characterized by the patterns of lymphokines they produce following activation (reviewed in Ref. I). Although these subsets were first identified by in vitro analysis of murine T-cell clones, strong evidence now exists for similar subsets in viva in mice, rats and humans. In mice, at least three CD4+ subsets exist: Th 1, Th2 and ThO. Thl cells secrete interleukin 2 (K-2), interferon y (IFN-y) and tumor necrosis factor (TNF), and support macrophage activation, delayed-type hypersensitivity (DTH) responses and immunoglobulin(Ig) isotype switching to IgG2a. Th2 cells secrete IL-4, II.-5, 11.-t;, IL-10 and IL-13, and provide efficient help for B-cell activation, for switching to the IgGl and IgE isotypes, and for antibody production. ThO cells are characterized by production of cytokines of both the Thl and Th2 types, and are thought to be obligatory precursors of Thl and Th2 cells.