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Although PKCθ-deficient T cells are hypo-responsive to peptide stimulation in vitro and in vivo, these two groups clearly demonstrate that anti-viral cytotoxic T lymphocyte responses in PKCθ-knockout mice are normal. It appears that additional signals from the innate immune system can compensate for the loss of PKCθ in T cells during pathogenic infections. Thus, PKCθ is not a crucial signalling molecule required for global T-mediated cell immune responses, as was previously thought.
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Berg-Brown N.N., Gronski M.A., Jones R.G., Elford A.R., Deenick E.K., Odermatt B., Littman D.R., and Ohashi P.S. PKCθ signals activation versus tolerance in vivo. J Exp Med 199 (2004) 743-752. Although PKCθ-deficient T cells are hypo-responsive to peptide stimulation in vitro and in vivo, these two groups clearly demonstrate that anti-viral cytotoxic T lymphocyte responses in PKCθ-knockout mice are normal. It appears that additional signals from the innate immune system can compensate for the loss of PKCθ in T cells during pathogenic infections. Thus, PKCθ is not a crucial signalling molecule required for global T-mediated cell immune responses, as was previously thought.
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•] both show that PKCθ is dispensable for Th1-mediated immune responses but is important for Th2 cell differentiation and function. However, purified naïve PKCθ-deficient T cells show enhanced IFNγ production during T cell activation, suggesting that PKCθ might well control some aspect of Th1 cell function. In this context, PKCθ regulates Th1 cytokine production in a model of experimental autoimmune encephalomyelitis [50]. How and why PKCθ regulates Th1/2 cell differentiation and/or function is not known.
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•] both show that PKCθ is dispensable for Th1-mediated immune responses but is important for Th2 cell differentiation and function. However, purified naïve PKCθ-deficient T cells show enhanced IFNγ production during T cell activation, suggesting that PKCθ might well control some aspect of Th1 cell function. In this context, PKCθ regulates Th1 cytokine production in a model of experimental autoimmune encephalomyelitis [50]. How and why PKCθ regulates Th1/2 cell differentiation and/or function is not known.
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