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J Neuropathol Exp Neurol. 1994 Jul;53(4):369-76.

Expression of cell adhesion molecules in inflammatory myopathies and Duchenne dystrophy.

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Neuromuscular Research Laboratory, Mayo Clinic, Rochester, Minnesota 55905.


Cell adhesion molecules participate in target-effector cell interactions in cell-mediated cytotoxicity and in leukodiapedesis in inflammatory diseases. Two ligand-receptor pairs may play a role in the adhesion of cytotoxic T cells to their targets: 1) intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1), and 2) LFA-3 and CD2. We therefore immunolocalized these molecules in myopathies where there is evidence for T cell-mediated myocytotoxicity, namely inclusion body myositis, polymyositis, and Duchenne dystrophy. Autoaggressive inflammatory cells close to invaded muscle fibers showed an increased expression of ICAM-1 and LFA-1. The nonnecrotic muscle fibers invaded by autoaggressive cells expressed ICAM-1 where their surfaces faced the invading cells. That immunoreactivity for ICAM-1 on the invading cells was distinct from that on the opposite muscle fiber surface was established by colocalization of ICAM-1 with the sarcolemmal marker dystrophin (or beta-spectrin) and was also confirmed by confocal microscopy. Leukodiapedesis in inflamed tissues is mediated by ICAM-1, LFA-3, vascular cell adhesion molecule-1 (VCAM-1), and E-selectin associated with endothelial cells. In dermatomyositis ICAM-1 was strongly expressed on endothelial cells of perimysial arterioles and venules and on some perifascicular capillaries. In all the other myopathies ICAM-1 and LFA-3 expressions were increased on endothelia of capillaries surrounded by inflammatory cells. VCAM-1 was detected in few arterioles in all diseases. E-selectin was not detected at any site in any disorder.(ABSTRACT TRUNCATED AT 250 WORDS).

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