Regulation of the immune response by nitric oxide differentially produced by T helper type 1 and T helper type 2 cells

TLDR

The balance between T helper type 1 (Th1) and T helper type 2 (Th2) cells determines the outcome of many important diseases. Using cloned murine T cell lines, the study shows that Th1, but not Th2, cells produce large amounts of nitric oxide (NO) upon activation, and that NO inhibits IL‑2 and interferon‑γ secretion by Th1 cells while having no effect on IL‑4 production by Th2 cells, thereby distinguishing Th1 and Th2 cells by differential NO production and susceptibility and indicating a self‑regulatory role of NO on Th1 cells implicated in immunopathology.

Abstract

Abstract The balance between T helper type 1 (Th1) and T helper type 2 (Th2) cells determines the outcome of many important diseases. Using cloned murine T cell lines, evidence is provided that Th 1, but not Th 2, cells can be activated by specific antigens or a T cell mitogen, concanavalin A, to produce large amounts of nitric oxide (NO). Furthermore, NO can inhibit the secretion of interleukin (IL)‐2 and interferon‐γ by Th 1 cells but has no effect on IL‐4 production by Th 2 cells. Th 1 and Th 2 cells can, thus, be distinguished by their differential production of and susceptibility to NO. NO exerts a self‐regulatory effect on Th 1 cells which are implicated in immunopathology.