Dauly C, Freret M, Drouot L, Ho J, Cosette P, Boyer O.
Application Note 555
Normal muscle fibers do not express detectable levels of class I major histocompatibility complex (MHC-I). In contrast, high-level expression of MHC-I is a hallmark of muscle autoimmune diseases such as polymyositis, inclusion-body myositis or dermatomyositis. It is generally considered that damage of muscle fibers in myositis results from an auto-immune attack by auto-reactive cytotoxic T lymphocytes (CTLs) that recognize muscle autoantigens presented by MHC-I molecules. We used a MHC-I–transgenic mouse model in which a controllable muscle-specific promoter governs the conditional up-regulation of a MHC-I molecule (H-2Kb) in skeletal muscle resulting in severe myopathy. A proteomic study was performed on mouse muscle tissue to evaluate the consequences of this forced H-2Kb expression. An experimental workflow was designed including protein digestion and label-free qualitative and quantitative analysis by high-resolution, accurate mass LC-MS/MS. Three muscle tissues from MHC-I–inducible mice were compared to two healthy controls using a differential analysis and targeted quantitation approach.
Thermo Fisher Scientific
United States
