Autor: |
Moingeon PE; Laboratory of Immunobiology, Dana-Farber Cancer Institute, Boston, MA 02115., Lucich JL, Stebbins CC, Recny MA, Wallner BP, Koyasu S, Reinherz EL |
Jazyk: |
angličtina |
Zdroj: |
European journal of immunology [Eur J Immunol] 1991 Mar; Vol. 21 (3), pp. 605-10. |
DOI: |
10.1002/eji.1830210311 |
Abstrakt: |
The influence of T cell receptor (TcR) triggering on T cell adhesion function has been systematically investigated in the present studies; we show that the adhesion function of LFA-1 is minimal in non-activated T cells but is augmented within minutes following TcR-mediated activation. In contrast, CD2 function is essentially optimal in non-activated T cells and undergoes no detectable modification within 12 h of TcR stimulation. Protein kinase C activation augments LFA-1 but not CD2 adhesion function and cyclic AMP reduces LFA-1 adhesion without affecting CD2-LFA-3 interactions. Up-regulation of the LFA-1 pathway occurs in the absence of any detectable surface redistribution of this molecule, suggesting an activation dependent modification leading to a high-affinity ICAM-1 binding state. The TcR independence of CD2 adhesion function implies a critical role of the CD2 pathway in initiating cell-cell interactions prior to TcR engagement and LFA-1-ICAM-1 binding and underscores the complementary nature of the CD2 and LFA-1 adhesion pathways during the immune response. |
Databáze: |
MEDLINE |
Externí odkaz: |
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