Cytokine-independent Jak3 Activation upon T Cell Receptor (TCR) Stimulation through Direct Association of Jak3 and the TCR Complex

Kazuhiro Tomita, Kaoru Saijo, Sho Yamasaki, Tomohiko Iida, Fubito Nakatsu, Hisashi Arase, Hiroshi Ohno, Takuji Shirasawa, Takayuki Kuriyama, John J. O'Shea, Takashi Saito

    Research output: Contribution to journalArticlepeer-review

    30 Citations (Scopus)

    Abstract

    Jak3 is responsible for growth signals by various cytokines such as interleukin (IL)-2, IL-4, and IL-7 through association with the common γ chain (γc) in lymphocytes. We found that T cells from Jak3-deficient mice exhibit impairment of not only cytokine signaling but also early activation signals and that Jak3 is phosphorylated upon T cell receptor (TCR) stimulation. TCR-mediated phosphorylation of Jak3 is independent of IL-2 receptor/γc but is dependent on Lck and ZAP-70. Jak3 was found to be assembled with the TCR complex, particularly through direct association with CD3ζ via its JH4 region, which is a different region from that for γc association. These results suggest that Jak3 plays a role not only in cell growth but also in T cell activation and represents cross-talk of a signaling molecule between TCR and growth signals.

    Original languageEnglish
    Pages (from-to)25378-25385
    Number of pages8
    JournalJournal of Biological Chemistry
    Volume276
    Issue number27
    DOIs
    Publication statusPublished - Jul 6 2001

    All Science Journal Classification (ASJC) codes

    • Biochemistry
    • Molecular Biology
    • Cell Biology

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