M2 polarized macrophages and giant cells contribute to myofibrosis in XXXX .

@entity1 @entity11602 @entity4094 @entity72965 @entity82 @entity738 @entity14452 @entity9656 @entity3840 @entity1198 @entity425 @entity5218 @entity842 @entity370 @entity925 @entity121
The etiopathogenesis of @entity370 , a systemic @entity738 , still remains obscure. A multitude of organs have been described to be affected in systemic @entity370 . Skeletal muscles may also be affected, leading to @entity925 and @entity425 . A workup of the specific immune response with emphasis on the macrophage response is provided herein. Affected muscle tissue from seven @entity1 with systemic @entity370 was analyzed and compared with that from seven @entity1 with other @entity121 containing macrophagocytic infiltration. Monocytes/macrophages and giant cells in granulomas of muscle tissue from @entity1 with @entity370 show a status of alternative activation (M2) based on their expression of @entity14452 , @entity5218 , @entity72965 as a consequence of a functionally type 2 helper T cell (Th2)-biased cytokine profile. Significant @entity82 and up-regulation of @entity11602 were associated with the M2 phenotype of macrophages. Conversely, up-regulated @entity1198 cytokines did not result in significant classical activation of macrophages (M1), with poor inducible @entity842 synthase and @entity3840 production. Giant cell formation was further associated with up-regulated expression of DNAX-activating protein of 12 kDa (DAP12; gene symbol @entity9656 ). Functionally, alternative activation of macrophages on the basis of a Th2-biased immune response may induce clinical symptoms and chronic evolution of @entity4094 . This is the first characterization of Th2-mediated immune mechanisms in @entity4094 suggesting that a specific macrophage activation status leading to myofibrosis may be a key event in the pathogenesis of this disease.
