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Evidence for MHC I–restricted CD8 + T‐cell–mediated immunopathology in canine masticatory muscle myositis and polymyositis
Author(s) -
Neumann J.,
Bilzer T.
Publication year - 2006
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.20456
Subject(s) - polymyositis , myositis , cd8 , major histocompatibility complex , autoantibody , myosin , antigen , immunology , myopathy , mhc class i , t cell , medicine , biology , antibody , pathology , immune system , microbiology and biotechnology
Masticatory muscle myositis (MMM) is the most common inflammatory myopathy (IM) in dogs, associated with antibodies against myosin. To further elucidate the immunopathogenesis, we investigated muscles of 53 dogs with MMM, 32 dogs with polymyositis (PM), and 4 dogs suffering from both, with regard to the presence and location of CD4 + and CD8 + T cells, B cells, macrophages, major histocompatibility complex (MHC) class I and class II antigens, and autoantibodies. CD8 + T cells were found in MMM (91%) and PM (75%), mostly paralleled (68% and 61%) by enhanced expression of MHC class I antigen on muscle fibers. CD8 + T cells invading intact and neighboring necrotic muscle fibers were present in MMM (39%) and PM (42%). Dogs with MMM lacking intramuscular (26%) and circulating (36%) autoantibodies also had CD8 + T‐cell infiltrations and muscle‐fiber lesions. Since MHC class I antigen and CD8 + T cells were detected in the presence of CD4 + T cells, regardless of antimuscular antibodies, we consider MMM and PM in the dog as a CD8 + T‐cell–mediated immunopathological disease that initiates muscle‐fiber destruction and leads to production of myosin autoantibodies. Muscle Nerve 2006