Abstract 2109 Allergy, Immunology, and Rheumatology Poster Symposium, Sunday, 5/2

T cell activation induces dramatic T cell cytoskeletal changes. There is increasing evidence that disruption of the cytoskeleton inhibits early and late events of T cell activation. However, little is known about which signaling molecules are involved in these cytoskeletal changes. The rho family of small GTP-binding proteins, which include rho, rac, and cdc42, regulate the cytoskeleton and coordinate various cellular functions via their many effector targets. In this study, we demonstrate that inactivation of rho by the Clostridium botulinum toxin, C3 exoenzyme, inhibits IL-2 transcription after stimulation through the CD3 complex. Inhibition of IL-2 expression correlated with loss of sustained increase in [Ca+2]i and mitogen activated protein kinase (MAPK/Erk) activity, but not with the activation of the T cell specific tyrosine kinase, lck. These findings are the first to show that rho is required for IL-2 production due, in part, to the requirement for sustained calcium influx and MAPK activation after antigen receptor ligation.

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