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TCR signaling induces selective exclusion of CD43 from the T cell-antigen-presenting cell contact site.
Sperling, A I; Sedy, J R; Manjunath, N; Kupfer, A; Ardman, B; Burkhardt, J K.
Afiliación
  • Sperling AI; Department of Medicine, University of Chicago, IL 60637, USA. asperlin@medicine.bsd.uchicago.edu
J Immunol ; 161(12): 6459-62, 1998 Dec 15.
Article en En | MEDLINE | ID: mdl-9862667
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.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Sialoglicoproteínas / Activación de Linfocitos / Receptores de Antígenos de Linfocitos T / Linfocitos T / Transducción de Señal / Antígenos CD / Membrana Celular / Células Presentadoras de Antígenos Límite: Humans Idioma: En Revista: J Immunol Año: 1998 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Sialoglicoproteínas / Activación de Linfocitos / Receptores de Antígenos de Linfocitos T / Linfocitos T / Transducción de Señal / Antígenos CD / Membrana Celular / Células Presentadoras de Antígenos Límite: Humans Idioma: En Revista: J Immunol Año: 1998 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos