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Acta Myol ; 27: 49-53, 2008 Oct.
Article in English | MEDLINE | ID: mdl-19364061

ABSTRACT

Distinct mechanisms such as humeral immunity in dermatomyositis (DM) and T-cell-mediated cytotoxicity in polymyositis (PM) contribute to the pathology of inflammatory myopathies. In addition, different subsets of macrophages are present in both diseases. Herein, the characteristics of 25F9-positive macrophages in skeletal muscle inflammation are outlined. Muscle biopsies of subjects with DM and PM were studied by immunohistochemical multi-labelling using the late-activation marker 25F9, together with markers characterizing macrophage function including IFN-gamma, iNOS, and TGF-beta. In PM, a robust expression of IFN-gamma, iNOS, and TGF-beta was observed in inflammatory cells. Double- and serial-labelling revealed that a subset of 25F9-positive macrophages in the vicinity of injured muscle fibres expressed iNOS and TGF-beta, but not IFN-gamma. In DM, IFN-gamma, iNOS and TGF-beta were also expressed in inflammatory cells in the endomysium. Double- and serial-labelling studies in DM indicated that 25F9-positive macrophages expressed TGF-beta and to a lesser degree iNOS, but not IFN-gamma. In conclusion, our data suggest that late-activated macrophages contribute to the pathology of inflammatory myopathies.


Subject(s)
Dermatomyositis/physiopathology , Macrophages/physiology , Polymyositis/physiopathology , Adult , Antigens, Differentiation, Myelomonocytic/metabolism , Child , Humans , Immunohistochemistry , Interferon-gamma/metabolism , Interferon-gamma/physiology , Macrophages/metabolism , Nitric Oxide Synthase Type II/metabolism , Nitric Oxide Synthase Type II/physiology , Transforming Growth Factor beta/metabolism , Transforming Growth Factor beta/physiology
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