Expression and Function of NADPH Oxidase(s) in T Lymphocytes

摘要

T cell receptor (TCR) signals induce ROS generation in T lymphocytes, and ROS regulate MAPK activation, apoptosis and gene expression, We have shown that T cells express a phagocyte-type NADPH oxidase and the absence of oxidase components leads to deficient TCR-induced ROS generation and altered T cell responses. NADPH oxidase-deficient T cells exhibited enhanced ERK activation and increased T_H1 cytokine secretion. Our data suggest that T cells also express the calcium-dependent, non-phagocytic oxidase Duoxl. Duoxl produces ROS early in TCR signaling and intracellular calcium flux is required, but not sufficient for TCR-induced ROS generation from Duox. These studies indicate role(s) for NADPH oxidase(s) in TCR induced ROS generation and suggest how T cell function may be altered in the absence of NADPH oxidase function.