Cutting edge: TCR signaling induces selective exclusion of CD43 from the T cell-antigen-presenting cell contact site

Anne I. Sperling, John R. Sedy, N. Manjunath, Abraham Kupfer, Blair Ardman, Janis K. Burkhardt

Research output: Contribution to journalArticle

Abstract

CD43, a large highly glycosylated molecule, is arguably the most abundant molecule on the surface of T cells. Nevertheless, the function of CD43 remains unclear. Utilizing fluorescence microscopy, we find that CD43 is excluded from the T cell-APC contact site. This exclusion is Ag dependent since optimal CD43 exclusion requires Ag-pulsed APC, and since signaling through CD3, in the absence of any other receptor ligand interactions, can induce the modulation of CD43. These data suggest that CD43 may function as a barrier to nonspecific T cell-APC interactions that is removed as a result of T cell activation. Exclusion from the interaction site is a unique feature of CD43 and not universally found for all large highly glycosylated molecules since CD45 is not excluded. Thus, CD43 may represent a novel regulatory molecule on the T cell surface that can direct T cell interactions by changing its location on the cell surface.

Original languageEnglish (US)
Pages (from-to)6459-6462
Number of pages4
JournalJournal of Immunology
Volume161
Issue number12
StatePublished - Dec 15 1998

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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    Sperling, A. I., Sedy, J. R., Manjunath, N., Kupfer, A., Ardman, B., & Burkhardt, J. K. (1998). Cutting edge: TCR signaling induces selective exclusion of CD43 from the T cell-antigen-presenting cell contact site. Journal of Immunology, 161(12), 6459-6462.