Cutting Edge: TCR Signaling Induces Selective Exclusion of CD43 from the T Cell-Antigen-Presenting Cell Contact Site

Author:

Sperling Anne I.12,Sedy John R.1,Manjunath N.3,Kupfer Abraham4,Ardman Blair3,Burkhardt Janis K.25

Affiliation:

1. *Section of Pulmonary and Critical Care Medicine of the Department of Medicine,

2. †Committee on Immunology, and

3. §Department of Medicine, Tupper Research Institute, Division of Hematology-Oncology, New England Medical Center Hospitals, Boston, MA 02111; and

4. ¶Division of Basic Science, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206

5. ‡Department of Pathology, University of Chicago, Chicago, IL 60637;

Abstract

AbstractCD43, 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.

Publisher

The American Association of Immunologists

Subject

Immunology,Immunology and Allergy

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