Enhancement of antigen-induced T-cell proliferation by soluble CD26/dipeptidyl peptidase IV.

DOI Web Site 被引用文献5件
  • T Tanaka
    Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA.
  • J S Duke-Cohan
    Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA.
  • J Kameoka
    Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA.
  • A Yaron
    Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA.
  • I Lee
    Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA.
  • S F Schlossman
    Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA.
  • C Morimoto
    Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA.

抄録

<jats:p>The addition of a soluble recombinant CD26 (sCD26) enhanced proliferation of peripheral blood lymphocytes induced by the recall antigen tetanus toxoid. sCD26 itself did not provide a mitogenic signal and did not augment the proliferative response of T cells to other mitogenic stimuli such as phytohemagglutinin and anti-CD3. Dipeptidyl peptidase IV-negative sCD26 did not have this enhancement effect, implying a requirement for enzyme activity. It was found that there exists a large variation in the levels of human plasma sCD26/dipeptidyl peptidase IV in vivo which may regulate T-cell activity. Peripheral blood lymphocytes from individuals whose plasma sCD26 was high and responded strongly to tetanus toxoid stimulation were insensitive to the enhancing effects of exogenously added sCD26. This suggests that plasma sCD26 had modulated the responsiveness of T cells of these individuals in vivo and that the endogenous plasma sCD26 regulates immune responses by allowing antigen-specific T cells to exert a maximal response to their specific antigen.</jats:p>

収録刊行物

被引用文献 (5)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ