Display Settings:


Send to:

Choose Destination
See comment in PubMed Commons below
Cell Immunol. 1993 Feb;146(2):249-60.

Function of dipeptidyl peptidase IV (CD26, Tp103) in transfected human T cells.

Author information

  • 1First Department of Medicine, University of Mainz, Germany.


CD26 (Tp103) is a proteolytic enzyme (dipeptidyl peptidase IV) expressed on the T cell surface that defines an alternative activation signal for human T lymphocytes. It is absent from or present in only low amounts on resting T cells but it is expressed strongly after activation. Crosslinking of CD26/Tp103 via the monoclonal antibody CB.1 triggers functional activities in preactivated T cells. To study the molecular requirements for T cell activation via CD26 we transfected a cDNA encoding CD26 into several CD26-negative cells. In Jurkat T cell leukemia cells that normally do not express the CD26 antigen, the transfected CD26 molecule is functional because the monoclonal antibody CB.1 induces an increase of cytosolic Ca2+ concentration and IL-2 production. For this stimulatory effect a crosslinking of the monoclonal antibody CB.1 is necessary. After modulation of the TCR/CD3 complex the transfected Jurkat cells were insensitive to triggering via CD26. Moreover, a CD26-transfected TCR-negative variant of Jurkat cells did not respond to CD26 triggering despite high levels of expression of the molecule on their surface. These data demonstrate that the function of CD26/Tp103 is dependent on the expression of the T cell receptor complex. In search of a physiological function of CD26 we found a costimulatory effect of mAb CB.1 in combination with the nonstimulatory anti-CD3 antibody BMA030 and an additive effect in the response to the superantigen staphylococcal enterotoxin E. Transfected Jurkat cells, however, did not show a reproducibly enhanced responsiveness to the superantigen compared to that of untransfected cells.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk