Chemokine production by rat myocytes exposed to interferon-γ

Messenger RNA that encodes for monocyte chemotactic protein-1 (MCP-1), as well as its protein product, was observed to be constitutively expressed at low levels in a monoclonal Lewis rat skeletal muscle cell line (LEI), Immunohistochemical analyses of sections of skeletal muscle yielded similar results. Since interferon-gamma (IFN-gamma) has been reported to have a likely role in determining the severity of symptoms in the neuromuscular autoimmune disease experimental myasthenia gravis (EAMG), the hypothesis tested and proven true in these studies was that IFN-gamma would up-regulate the production of MCP-I in LE1 cells. It was also observed that muscle-derived MCP-1 could be up-regulated in vivo in rats receiving a monoclonal anti-acetylcholine receptor antibody (mAb35), a potent inducer of symptoms of EAMG. Therefore, it is concluded that muscle may contribute to disease progression by producing factors that influence activities of the immune system. (C) 2000 Academic Press.