Interleukin-17 increases the effects of IL-1 beta on muscle cells: arguments for the role of T cells in the pathogenesis of myositis.

We studied the production of interleukin (IL)-6 and CCL20/macrophage inflammatory protein-3 alpha (MIP-3 alpha) by human myoblasts and muscle samples in response to IL-17 alone or in combination with IL-1 beta. Both IL-17 and IL-1 beta induced IL-6 production by normal myoblasts and muscle samples. IL-17 had no effect on CCL20 production by myoblasts. Combination of IL-17 and IL-1 beta further increased IL-6 and CCL20 production by muscle samples but not that of CK. IL-17 induced also HLA class I, C-Fos, nuclear factor kappa B (NF-kappa B) and C-Jun expression by myoblasts but not that of HLA class II, CD40, vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1). Finally, immunostaining of dermatomyositis (DM) and polymyositis (PM) muscle biopsies showed IL-17 and CCL20 expression. Our study shows that low levels of cytokines produced by T cells (IL-17) and monocytes (IL-1 beta) can act in combination on skeletal myoblasts and muscle tissue.