Complementary roles for CD2 and LFA-1 adhesion pathways during T cell activation

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Abstract
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.