PKC-θ is required for TCR-induced NF-κB activation in mature but not immature T lymphocytes

Zuoming Sun, Christopher W. Arendt, Wilfried Ellmeier, Edward M. Schaeffer, Mary Jean Sunshine, Leena Gandhi, Justin Annes, Daniela Petrzilka, Abraham Kupfer, Pamela L. Schwartzberg and Dan R. Littman ()
Additional contact information
Zuoming Sun: Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine
Christopher W. Arendt: Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine
Wilfried Ellmeier: Howard Hughes Medical Institute
Edward M. Schaeffer: National Human Genome Research Institute, National Institutes of Health
Mary Jean Sunshine: Howard Hughes Medical Institute
Leena Gandhi: Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine
Justin Annes: Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine
Daniela Petrzilka: Howard Hughes Medical Institute
Abraham Kupfer: National Jewish Medical and Research Center
Pamela L. Schwartzberg: National Human Genome Research Institute, National Institutes of Health
Dan R. Littman: Howard Hughes Medical Institute

Nature, 2000, vol. 404, issue 6776, 402-407

Abstract: Abstract Productive interaction of a T lymphocyte with an antigen-presenting cell results in the clustering of the T-cell antigen receptor (TCR) and the recruitment of a large signalling complex to the site of cell–cell contact1,2. Subsequent signal transduction resulting in cytokine gene expression requires the activation of one or more of the multiple isoenzymes of serine/threonine-specific protein kinase C (PKC)3. Among the several PKC isoenzymes expressed in T cells, PKC-θ is unique in being rapidly recruited to the site of TCR clustering4. Here we show that PKC-θ is essential for TCR-mediated T-cell activation, but is dispensable during TCR-dependent thymocyte development. TCR-initiated NF-κB activation was absent from PKC-θ-/- mature T lymphocytes, but was intact in thymocytes. Activation of NF-κB by tumour-necrosis factor α and interleukin-1 was unaffected in the mutant mice. Although studies in T-cell lines had suggested that PKC-θ regulates activation of the JNK signalling pathway5,6, induction of JNK was normal in T cells from mutant mice. These results indicate that PKC-θ functions in a unique pathway that links the TCR signalling complex to the activation of NF-κB in mature T lymphocytes.

Date: 2000
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DOI: 10.1038/35006090

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