Abstract
The chemokine monokine induced by interferon (IFN)-γ (MIG) is expressed in idiopathic inflammatory myopathies muscle. Abundant expression of MIG was observed on macrophages and T cells surrounding and invading non-necrotic muscle fibers in polymyositis and in inclusion-body myositis and in T cells in perimysial infiltrates of dermatomyositis. MIG is also localized to blood vessel endothelial cells in all inflammatory and normal muscle tissues and it exerts its biological effects mainly via binding to the chemokine (C-X-C motif) receptor (CXCR)3. Serum MIG is high in patients with inflammatory myopathies. Human skeletal muscle cells might actively self-promote muscular inflammation by eliciting MIG secretion, under the influence of cytokines (IFN-γ, tumor necrosis factor-α), which can amplify Th1 cell tissue infiltration in vivo. It has been shown that drugs able to block the MIG/CXCR3 axis can suppress inflammation in muscle.
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