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Joint-Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN) and the Scandinavian Neuropathological Society (SNS)

German Society for Neuropathology and Neuroanatomy

22.09.-24.09.2016, Hamburg

Diagnostic Value of myocytic MHC-II expression in Canine immune-mediated Myositis (CIMM)

Meeting Abstract

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  • presenting/speaker Marco Rosati - Faculty of Veterinary Medicine LMU Munich, Section of Clinical & Comparative Neuropathology and Neurology, Munich, Germany
  • Miriam Leipig - Faculty of Veterinary Medicine LMU Munich, Section of Clinical & Comparative Neuropathology and Neurology, Munich, Germany
  • Kaspar Matiasek - Faculty of Veterinary Medicine LMU Munich, Section of Clinical & Comparative Neuropathology and Neurology, Munich, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. Scandinavian Neuropathological Society. Joint-Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN) and the Scandinavian Neuropathological Society (SNS). Hamburg, 22.-24.09.2016. Düsseldorf: German Medical Science GMS Publishing House; 2016. Doc16dgnnP26

doi: 10.3205/16dgnn32, urn:nbn:de:0183-16dgnn329

Published: September 14, 2016

© 2016 Rosati et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

Text

CIMM is represented by two major subtypes: masticatory muscle myositis (MMM) and polymyositis (PM). Immunotherapy is the mainstay of CIMM treatment and it is therefore mandatory to achieve a definite diagnosis with exclusion of infective aetiologies beforehand. Lymphocytic invasion of predegenerate myofibres is the hallmark of CIMM but patchy lesion distribution and preceding treatment may interfere with detection of immune cell infiltrates on microscopy. Use of immunohistochemical markers, such as MHC-I and MHC-II, has been implemented to increase diagnostic accuracy of muscle biopsy investigation in few studies. Since myocytes may act as antigen-presenting cells, their MHC-II expression was evaluated as add-on tool for CIMM diagnosis.

Expression of CD3, CD8, CD20, IBA-1 and MHC-II was evaluated in muscle biopsies of 34 CIMM dogs, 10 dogs with non-inflammatory myopathy and 10 dogs with denervation muscle atrophy. The expression was semiquantitatively scored (all markers) and sorted for cellular and subcellular distribution (MHC-II) after which group specific data were processed according to standard algorithms.

Inflammatory infiltrates were observed in all CIMM. Overall, myocytic MHC-II expression was significantly increased in CIMM if compared to the other groups (p≤0.02), which only stained weakly positive in up to 35% of cases. There was a moderate correlation (0.52; p=0.01) between CD3 and MHC-II for CIMM cases. 11.7% of CIMM did neither show sarcolemmal nor sarcoplasmic MHC-II immunoreactivity. However, with a cut off at score 2, myocytic MHC-II expression reached 100% specificity and 75% sensitivity with 23/34 (67.6%). The overall calculated accuracy was 83%.

Myocytic MHC-II expression proved to be a valuable marker for CIMM diagnosis that extends beyond inflammatory foci. Subthreshold MHC-II expression in spite of inflammatory infiltrates requires careful interpretation of MHC-II immunohistochemistry. Immunosuppressive treatment prior to biopsy collection might have influenced MHC-II expression results.