© 1996 British Society for Rheumatology
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T-LYMPHOCYTE IMMUNOPHENOTYPING IN POLYMYOSITIS AND DERMATOMYOSITIS
Rheumatology Unit, Guy's Hospital Arthur Stanley House, London
*Bloomsbury Rheumatology Unit Arthur Stanley House, London
Correspondence to:
Correspondence to: G. S. Panayi, ARC Professor of Rheumatology, Rheumatology Unit, Guy's Hospital, 4th Floor, Hunts House, London SE1 9RT.
The objective was to elucidate the immunological abnormalities underlying polymyositis (PM) and dermatomyositis (DM). The phenotype of peripheral blood mononuclear cell (PBMNC) subsets and cell surface expression of activation (CD25 and HLA-DR) and adhesion (LFA-1) molecules was studied in 12 patients with PM and in 10 patients with DM. PBMNC subsets and expression of T-cell activation molecules were evaluated by cytofluorography. Double immunofluorescence and indirect immunoperoxidase techniques were applied to muscle biopsies to define T-cell phenotype and LFA-1/ICAM-1 expression. In PM, the absolute number of circulating cytotoxic (CD8 + CD28+) T cells was selectively reduced. T cells showed-increased expression of activation molecules, CD25 and HLA-DR, and increased adhesion capacity as the absolute numbers of CD3 + CD25 +, CD8 + HLA-DR+, CD3 + LFA-1 +"bright" and CD8 LFA-1 +"bright" cells were higher than in healthy donors and DM patients. In PM muscle biopsies, T cells were mainly CD3 + CD8 + and LFA-1 +; additionally, endothelial cells and myofibres surrounded by T cells showed positive staining for ICAM-1. In DM, there was a general rymphopenia that led to a decreased absolute number of all T-lymphocyte subsets. It is proposed that in PM, in contrast to DM, LFA-1/ICAM-1 interactions enable activated CD8 + T cells to migrate selectively into the inflamed muscle and to adhere to myofibres, leading to tissue injury
KEY WORDS: CD8, CD28, LFA-1, ICAM-1, Polymyositis, Dermatomyositis
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