Evidence for MHC I-restricted CD8+ T-cell-mediated immunopathology in canine masticatory muscle myositis and polymyositis

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...

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Veröffentlicht in:Muscle & nerve 2006-02, Vol.33 (2), p.215-224
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description 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
doi_str_mv 10.1002/mus.20456
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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. 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Psychology ; Genes, MHC Class I ; Genes, MHC Class II ; immunoglobulin ; Immunoglobulin G - analysis ; Immunohistochemistry ; Immunophenotyping ; inflammatory myopathy ; Macrophages - immunology ; Macrophages - pathology ; Major Histocompatibility Complex - genetics ; Major Histocompatibility Complex - immunology ; Major Histocompatibility Complex - physiology ; major histocompatibility complex I ; Male ; masticatory muscle myositis ; Masticatory Muscles - immunology ; Masticatory Muscles - physiopathology ; Medical sciences ; MHC class I antigen ; muscle autoantibodies ; Muscle Fibers, Skeletal - immunology ; Muscle Fibers, Skeletal - pathology ; Myosins - immunology ; Myositis - immunology ; Myositis - physiopathology ; Myositis - veterinary ; Neurology ; polymyositis ; Polymyositis - immunology ; Polymyositis - physiopathology ; Polymyositis - veterinary ; Striated muscle. 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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</description><subject>Animals</subject><subject>Autoantibodies - immunology</subject><subject>B-Lymphocytes - immunology</subject><subject>B-Lymphocytes - pathology</subject><subject>Biological and medical sciences</subject><subject>canine myopathy</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4-Positive T-Lymphocytes - pathology</subject><subject>CD4-Positive T-Lymphocytes - physiology</subject><subject>CD8+ T cells</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - pathology</subject><subject>Diseases of striated muscles. 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Psychology</subject><subject>Genes, MHC Class I</subject><subject>Genes, MHC Class II</subject><subject>immunoglobulin</subject><subject>Immunoglobulin G - analysis</subject><subject>Immunohistochemistry</subject><subject>Immunophenotyping</subject><subject>inflammatory myopathy</subject><subject>Macrophages - immunology</subject><subject>Macrophages - pathology</subject><subject>Major Histocompatibility Complex - genetics</subject><subject>Major Histocompatibility Complex - immunology</subject><subject>Major Histocompatibility Complex - physiology</subject><subject>major histocompatibility complex I</subject><subject>Male</subject><subject>masticatory muscle myositis</subject><subject>Masticatory Muscles - immunology</subject><subject>Masticatory Muscles - physiopathology</subject><subject>Medical sciences</subject><subject>MHC class I antigen</subject><subject>muscle autoantibodies</subject><subject>Muscle Fibers, Skeletal - immunology</subject><subject>Muscle Fibers, Skeletal - pathology</subject><subject>Myosins - immunology</subject><subject>Myositis - immunology</subject><subject>Myositis - physiopathology</subject><subject>Myositis - veterinary</subject><subject>Neurology</subject><subject>polymyositis</subject><subject>Polymyositis - immunology</subject><subject>Polymyositis - physiopathology</subject><subject>Polymyositis - veterinary</subject><subject>Striated muscle. 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Tendons</topic><topic>Vertebrates: osteoarticular system, musculoskeletal system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Neumann, J.</creatorcontrib><creatorcontrib>Bilzer, T.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Muscle &amp; nerve</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Neumann, J.</au><au>Bilzer, T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence for MHC I-restricted CD8+ T-cell-mediated immunopathology in canine masticatory muscle myositis and polymyositis</atitle><jtitle>Muscle &amp; nerve</jtitle><addtitle>Muscle Nerve</addtitle><date>2006-02</date><risdate>2006</risdate><volume>33</volume><issue>2</issue><spage>215</spage><epage>224</epage><pages>215-224</pages><issn>0148-639X</issn><eissn>1097-4598</eissn><coden>MUNEDE</coden><abstract>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</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>16270307</pmid><doi>10.1002/mus.20456</doi><tpages>10</tpages></addata></record>
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subjects Animals
Autoantibodies - immunology
B-Lymphocytes - immunology
B-Lymphocytes - pathology
Biological and medical sciences
canine myopathy
CD4-Positive T-Lymphocytes - immunology
CD4-Positive T-Lymphocytes - pathology
CD4-Positive T-Lymphocytes - physiology
CD8+ T cells
CD8-Positive T-Lymphocytes - immunology
CD8-Positive T-Lymphocytes - pathology
Diseases of striated muscles. Neuromuscular diseases
dog
Dog Diseases - immunology
Dog Diseases - physiopathology
Dogs
Female
Fundamental and applied biological sciences. Psychology
Genes, MHC Class I
Genes, MHC Class II
immunoglobulin
Immunoglobulin G - analysis
Immunohistochemistry
Immunophenotyping
inflammatory myopathy
Macrophages - immunology
Macrophages - pathology
Major Histocompatibility Complex - genetics
Major Histocompatibility Complex - immunology
Major Histocompatibility Complex - physiology
major histocompatibility complex I
Male
masticatory muscle myositis
Masticatory Muscles - immunology
Masticatory Muscles - physiopathology
Medical sciences
MHC class I antigen
muscle autoantibodies
Muscle Fibers, Skeletal - immunology
Muscle Fibers, Skeletal - pathology
Myosins - immunology
Myositis - immunology
Myositis - physiopathology
Myositis - veterinary
Neurology
polymyositis
Polymyositis - immunology
Polymyositis - physiopathology
Polymyositis - veterinary
Striated muscle. Tendons
Vertebrates: osteoarticular system, musculoskeletal system
title Evidence for MHC I-restricted CD8+ T-cell-mediated immunopathology in canine masticatory muscle myositis and polymyositis
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