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Publication : Differential regulation of Th2 and Th1 lung inflammatory responses by protein kinase C theta.

First Author  Salek-Ardakani S Year  2004
Journal  J Immunol Volume  173
Issue  10 Pages  6440-7
PubMed ID  15528385 Mgi Jnum  J:94285
Mgi Id  MGI:3511742 Doi  10.4049/jimmunol.173.10.6440
Citation  Salek-Ardakani S, et al. (2004) Differential regulation of Th2 and Th1 lung inflammatory responses by protein kinase C theta. J Immunol 173(10):6440-7
abstractText  In vitro and recent in vivo studies have identified protein kinase Ctheta (PKCtheta) as an important intermediate in signaling pathways leading to T cell activation, proliferation, and cytokine production. However, the importance of PKCtheta to many T cell-driven inflammatory responses has not been demonstrated. In this study we show that although PKCtheta is required for the development of a robust lung inflammatory response controlled by Th2 cells, it plays a lesser role in the development of a similar lung inflammatory response controlled by Th1 cells. PKCtheta-deficient mice were strongly compromised in generating Th2 cells and exhibited reduced airway eosinophilia and Th2 cytokine production in lungs. PKCtheta was required for the initial development of Th1 cells, with these cells exhibiting delayed kinetics of differentiation and accumulation. However, with recall Ag challenge via the airways, this defect was overcome, and lung infiltration and Th1 cytokine production were largely unimpaired in PKCtheta-deficient animals. These data suggest that PKCtheta can play roles in aspects of both Th2 and Th1 responses, but lung inflammation induced by Th2 cells is more dependent on this protein kinase than lung inflammation induced by Th1 cells.
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