Essential Role of NF-κB-Inducing Kinase in T Cell Activation Through the TCR/CD3 Pathway

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  • Mitsuru Matsumoto
    Division of Molecular Immunology, Institute for Enzyme Research, University of Tokushima , Tokushima ,
  • Takuji Yamada
    First Department of Internal Medicine, School of Medicine, Ehime University , Ehime ,
  • Steven K Yoshinaga
    Amgen , Thousand Oaks, CA 91320
  • Tom Boone
    Amgen , Thousand Oaks, CA 91320
  • Tom Horan
    Amgen , Thousand Oaks, CA 91320
  • Shigeru Fujita
    First Department of Internal Medicine, School of Medicine, Ehime University , Ehime ,
  • Yi Li
    Division of Molecular Immunology, Institute for Enzyme Research, University of Tokushima , Tokushima ,
  • Tasuku Mitani
    Division of Molecular Immunology, Institute for Enzyme Research, University of Tokushima , Tokushima ,

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公開日
2002-08-01
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.169.3.1151
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>NF-κB-inducing kinase (NIK) is involved in lymphoid organogenesis in mice through lymphotoxin-β receptor signaling. To clarify the roles of NIK in T cell activation through TCR/CD3 and costimulation pathways, we have studied the function of T cells from aly mice, a strain with mutant NIK. NIK mutant T cells showed impaired proliferation and IL-2 production in response to anti-CD3 stimulation, and these effects were caused by impaired NF-κB activity in both mature and immature T cells; the impaired NF-κB activity in mature T cells was also associated with the failure of maintenance of activated NF-κB. In contrast, responses to costimulatory signals were largely retained in aly mice, suggesting that NIK is not uniquely coupled to the costimulatory pathways. When NIK mutant T cells were stimulated in the presence of a protein kinase C (PKC) inhibitor, proliferative responses were abrogated more severely than in control mice, suggesting that both NIK and PKC control T cell activation in a cooperative manner. We also demonstrated that NIK and PKC are involved in distinct NF-κB activation pathways downstream of TCR/CD3. These results suggest critical roles for NIK in setting the threshold for T cell activation, and partly account for the immunodeficiency in aly mice.</jats:p>

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