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1
Divisions of
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Molecular Immunology and
Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121
In vitro and recent in vivo studies have identified protein kinase C
(PKC) as an important intermediate in signaling pathways leading to T cell activation, proliferation, and cytokine production. However, the importance of PKC to many T cell-driven inflammatory responses has not been demonstrated. In this study we show that although PKC 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. PKC-deficient mice were strongly compromised in generating Th2 cells and exhibited reduced airway eosinophilia and Th2 cytokine production in lungs. PKC 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 PKC-deficient animals. These data suggest that PKC 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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