DOCK2 is essential for antigen-induced translocation of TCR and lipid rafts, but not PKC-θ and LFA-1, in T cells

Terukazu Sanui, Ayumi Inayoshi, Mayuko Noda, Eiko Iwata, Masahiro Oike, Takehiko Sasazuki, Yoshinori Fukui

研究成果: Contribution to journalArticle査読

97 被引用数 (Scopus)

抄録

DOCK2 is a mammalian homolog of Caenorhabditis elegans CED-5 and Drosophila melanogaster Myoblast City which are known to regulate actin cytoskeleton. DOCK2 is critical for lymphocyte migration, yet the role of DOCK2 in TCR signaling remains unclear. We show here that DOCK2 is essential for TCR-mediated Rac activation and immunological synapse formation. In DOCK2-deficient T cells, antigen-induced translocation of TCR and lipid rafts, but not PKC-θ and LFA-1, to the APC interface was severely impaired, resulting in a significant reduction of antigen-specific T cell proliferation. In addition, we found that the efficacy of both positive and negative selection was reduced in DOCK2-deficient mice. These results suggest that DOCK2 regulates T cell responsiveness through remodeling of actin cytoskeleton via Rac activation.

本文言語英語
ページ(範囲)119-129
ページ数11
ジャーナルImmunity
19
1
DOI
出版ステータス出版済み - 7 1 2003

All Science Journal Classification (ASJC) codes

  • 免疫アレルギー学
  • 免疫学
  • 感染症

フィンガープリント

「DOCK2 is essential for antigen-induced translocation of TCR and lipid rafts, but not PKC-θ and LFA-1, in T cells」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル