Loss of Protein Kinase Ctheta, Bcl10, or Malt1 Selectively Impairs Proliferation and NF-kappaB Activation in the CD4+ T Cell Subset Export

@article{citeulike:3433317, abstract = {The cytosolic proteins protein kinase C{theta} (PKC{theta}), Bcl10, and Malt1 play critical roles in TCR signaling to the transcription factor NF-{kappa}B. Our data confirm that CD4+ T cells from PKC{theta}, 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-{kappa}B activation, whereas NF-{kappa}B activation is only partially impaired in CD8+ T cells. Overall, our results suggest that defects in TCR signaling through PKC{theta}, Bcl10, and Malt1 predominantly impair NF-{kappa}B activation and downstream functional responses of CD4+ T cells. In contrast, CD8+ T cells maintain substantial NF-{kappa}B signaling, implying the existence of a significant TCR-regulated NF-{kappa}B activation pathway in CD8+ T cells that is independent of PKC{theta}, Bcl10, and Malt1.}, author = {Kingeter, Lara M. and Schaefer, Brian C.}, citeulike-article-id = {3433317}, citeulike-linkout-0 = {http://www.jimmunol.org/cgi/content/abstract/181/9/6244}, day = {1}, journal = {J Immunol}, keywords = {bcl10, malt1, nfkb, pkctheta}, month = {November}, number = {9}, pages = {6244--6254}, posted-at = {2008-10-21 12:48:47}, priority = {2}, title = {Loss of Protein Kinase C{theta}, Bcl10, or Malt1 Selectively Impairs Proliferation and NF-{kappa}B Activation in the CD4+ T Cell Subset}, url = {http://www.jimmunol.org/cgi/content/abstract/181/9/6244}, volume = {181}, year = {2008} }

TY - JOUR ID - citeulike:3433317 L3 - citeulike-article-id:3433317 N2 - The cytosolic proteins protein kinase C{theta} (PKC{theta}), Bcl10, and Malt1 play critical roles in TCR signaling to the transcription factor NF-{kappa}B. Our data confirm that CD4+ T cells from PKC{theta}, 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-{kappa}B activation, whereas NF-{kappa}B activation is only partially impaired in CD8+ T cells. Overall, our results suggest that defects in TCR signaling through PKC{theta}, Bcl10, and Malt1 predominantly impair NF-{kappa}B activation and downstream functional responses of CD4+ T cells. In contrast, CD8+ T cells maintain substantial NF-{kappa}B signaling, implying the existence of a significant TCR-regulated NF-{kappa}B activation pathway in CD8+ T cells that is independent of PKC{theta}, Bcl10, and Malt1. IS - 9 JF - J Immunol EP - 6254 TI - Loss of Protein Kinase C{theta}, Bcl10, or Malt1 Selectively Impairs Proliferation and NF-{kappa}B Activation in the CD4+ T Cell Subset VL - 181 SP - 6244 KW - bcl10 KW - malt1 KW - nfkb KW - pkctheta AU - Kingeter, Lara AU - Schaefer, Brian PY - 2008/11/01/ UR - http://www.jimmunol.org/cgi/content/abstract/181/9/6244 ER -