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CUTTING EDGE |
,
*
Section of Pulmonary and Critical Care Medicine of the Department of Medicine,
Committee on Immunology, and
Department of Pathology, University of Chicago, Chicago, IL 60637;
§
Department of Medicine, Tupper Research Institute, Division of Hematology-Oncology, New England Medical Center Hospitals, Boston, MA 02111; and
¶
Division of Basic Science, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206
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.
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