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Sci. Signal., 3 August 2010
Vol. 3, Issue 133, p. ra59
[DOI: 10.1126/scisignal.2000976]


Editor's Summary

Oxidative Feedback
Reactive oxygen species (ROS) are formed as unwanted by-products of cellular respiration and have deleterious effects, such as causing tissue damage. However, ROS also have beneficial uses—for example, in the destruction of pathogens by phagocytic cells. ROS also enhance T cell receptor (TCR) responses; however, the source of ROS and the mechanism by which ROS modulate signaling in T cells are unclear. Kwon et al. show that stimulation of the TCR in human CD4+ T cells activates the Ca2+-dependent, nonphagocytic NADPH oxidase Duox1 to generate ROS in a manner that depends on TCR-proximal kinases. ROS enhanced TCR signaling in a positive feedback loop by inhibiting the inactivation of a key TCR-dependent kinase called ZAP-70. Knockdown of Duox1 inhibited signaling downstream of the TCR and the production of cytokines. Together with other studies of the effects of ROS on B cells, these data suggest that ROS are functionally important in nonphagocytic cells of the immune system.

Citation: J. Kwon, K. E. Shatynski, H. Chen, S. Morand, X. de Deken, F. Miot, T. L. Leto, M. S. Williams, The Nonphagocytic NADPH Oxidase Duox1 Mediates a Positive Feedback Loop During T Cell Receptor Signaling. Sci. Signal. 3, ra59 (2010).

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