T cell interactions with laminin, the major glycoprotein of the basement membrane, are important in lymphocyte migration in the cutaneous inflammatory response (1-4). However, the interactions of lymphocytes with laminin are only beginning to be understood. Underlying the proposed studies is our finding that the 67 kD laminin binding protein (p67 LBP) is expressed on the surface of activated but not resting T lymphocytes. We initially identified p67 LBP by the differential expression of the mRNA encoding its polypeptide precursor, p37 LBPP, in a pair of T cell tumor line subclones that represent phenotypic characteristics of either resting or activated T cells. Subsequently, suing the anti-p67 LBP monoclonal antibody (mAb) MLuC5(6), we demonstrated that p67 LBP is expressed on activated memory T cells, and not expressed on naive or resting cells. The present grant addresses the T cell requirements for p67 LBP expression, the nature of the subset of T lymphocytes which express p67 LBP, and the role that p67 LBP plays in T cell migration into the skin. The long term objective of these studies is to define the role of p67 LBP in cutaneous T cell homing, and to identify potential therapeutic targets in the treatment of immune- mediated skin disease. We propose to address the following specific aims: 1. What stimuli induce the expression of p67 LBP on normal T cell? 2. What is the phenotype of the p67 LBP-expressing T cell subset with respect to the T lymphocytes known to traffic to the skin? 3. Do the T cells infiltrating cutaneous sites of inflammation express p67 LBP?
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