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• W2067206927 endingPage "6254" @default.
• W2067206927 startingPage "6244" @default.
• W2067206927 abstract "Abstract The cytosolic proteins protein kinase Cθ (PKCθ), Bcl10, and Malt1 play critical roles in TCR signaling to the transcription factor NF-κB. Our data confirm that CD4+ T cells from PKCθ, Bcl10, and Malt1 knockout mice show severe impairment of proliferation in response to TCR stimulation. Unexpectedly, we find that knockout CD8+ T cells proliferate to a similar extent as wild-type cells in response to strong TCR signals, although a survival defect prevents their accumulation. Both CD4+ and CD8+ knockout T cells express activation markers, including CD25, following TCR stimulation. Addition of exogenous IL-2 rescues survival of knockout CD4+ and CD8+ T cells, but fails to overcome the proliferation defect of CD4+ T cells. CD4+ T cells from knockout mice are extremely deficient in TCR-induced NF-κB activation, whereas NF-κB activation is only partially impaired in CD8+ T cells. Overall, our results suggest that defects in TCR signaling through PKCθ, Bcl10, and Malt1 predominantly impair NF-κB activation and downstream functional responses of CD4+ T cells. In contrast, CD8+ T cells maintain substantial NF-κB signaling, implying the existence of a significant TCR-regulated NF-κB activation pathway in CD8+ T cells that is independent of PKCθ, Bcl10, and Malt1." @default.
• W2067206927 created "2016-06-24" @default.
• W2067206927 creator A5004362492 @default.
• W2067206927 creator A5005095682 @default.
• W2067206927 date "2008-11-01" @default.
• W2067206927 modified "2023-10-16" @default.
• W2067206927 title "Loss of Protein Kinase Cθ, Bcl10, or Malt1 Selectively Impairs Proliferation and NF-κB Activation in the CD4+ T Cell Subset" @default.
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• W2067206927 doi "https://doi.org/10.4049/jimmunol.181.9.6244" @default.
• W2067206927 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2630173" @default.
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