Attenuation of experimental autoimmune myositis by blocking ICOS-ICOS ligand interaction.

摘要: Polymyositis (PM) is an acquired, systemic, connective tissue disease characterized by the proximal muscle weakness and infiltration of mononuclear cells into affected muscles. To understand its etiology immunopathogenesis, appropriate animal model required. It has been demonstrated that immunization with native human skeletal C protein induces severe reproducible experimental autoimmune myositis (EAM) in Lewis rats, inflammatory lesions EAM mimic those PM. In present study, we prepared recombinant fragment succeeded inducing as protein. We found ICOS expression on fiber-infiltrating T but not normal rats. Treatment anti-ICOS mAb reduced incidence severity myositis; decreased number muscle-infiltrating CD11b/c + , TCR CD8a cells; inhibited IL-1α CCL2 hamstring muscles However, treatment neither serum anti-C IgG level, protein-induced proliferation lymph node (LN) cells, or LN nor production IFN-γ protein-stimulated These data indicate analysis provides only insights pathogenesis PM, also useful information regarding development effective immunotherapy against disease. ICOS-ICOS ligand interaction would be a novel therapeutic target for