Abstract
The α-chemokines (C-X-C motif) ligand 9 (CXCL9) and interferon γ-induced protein 10 (IP-10) are expressed in idiopathic inflammatory myopathies muscle. Abundant expression of IP-10 was observed on macrophages and T cells surrounding and invading non-necrotic muscle fibers in polymyositis and sporadic inclusion body myositis and in T cells in perimysial infiltrates of dermatomyositis. IP-10 was also localized to blood vessel endothelial cells in all inflammatory and normal muscle tissues. Serum IP-10 is high in patients with inflammatory myopathies. Human skeletal muscle cells might actively self-promote muscular inflammation by eliciting IP-10 secretion, under the influence of cytokines [Interferon (IFN-γ), Tumor Necrosis Factor (TNF-α)], which can amplify T helper (Th)1 cell tissue infiltration in vivo. It has been shown that drugs able to block the IP-10/chemokine (C-X-C motif) receptor 3 (CXCR3) axis can suppress inflammation in muscle.
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