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The Journal of Immunology, 2006, 176: 6004-6011.
Copyright © 2006 by The American Association of Immunologists

Defective IgG2a/2b Class Switching in PKC{alpha}–/– Mice1

Christa Pfeifhofer*, Thomas Gruber*, Thomas Letschka*, Nikolaus Thuille*, Christina Lutz-Nicoladoni*, Natascha Hermann-Kleiter1, Uschi Braun{dagger}, Michael Leitges2,{dagger} and Gottfried Baier2,3,*

* Department for Medical Genetics, Molecular and Clinical Pharmacology, Medical University, Innsbruck, Austria; and {dagger} Department of Experimental Endocrinology, Medical University, Hanover, Germany

Using model tumor T cell lines, protein kinase C (PKC) {alpha} has been implicated in IL-2 cytokine promoter activation in response to Ag receptor stimulation. In this study, for the first time, PKC{alpha} null mutant mice are analyzed and display normal T and B lymphocyte development. Peripheral CD3+ PKC{alpha}-deficient T cells show unimpaired activation-induced IL-2 cytokine secretion, surface expression of CD25, CD44, and CD69, as well as transactivation of the critical transcription factors NF-AT, NF-{kappa}B, AP-1, and STAT5 in vitro. Nevertheless, CD3/CD28 Ab- and MHC alloantigen-induced T cell proliferation and IFN-{gamma} production are severely impaired in PKC{alpha}–/– CD3+ T cells. Consistently, PKC{alpha}-deficient CD3+ T cells from OVA-immunized PKC{alpha}-deficient mice exhibit markedly reduced recall proliferation to OVA in in vitro cultures. In vivo, PKC{alpha}-deficient mice give diminished OVA-specific IgG2a and IgG2b responses following OVA immunization experiments. In contrast, OVA-specific IgM and IgG1 responses and splenic PKC{alpha}–/– B cell proliferation are unimpaired. Our genetic data, thus, define PKC{alpha} as the physiological and nonredundant PKC isotype in signaling pathways that are necessary for T cell-dependent IFN-{gamma} production and IgG2a/2b Ab responses.




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