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THU0062 The Potential Role of Mast Cells in the C-Protein Induced Myositis Model
  1. K. Shin1,
  2. J. Y. Choi2,
  3. S. H. Chang2,
  4. Y. W. Song2
  1. 1Division of Rheumatology, Department of Internal Medicine, SMG-SNU Boramae Medical Center
  2. 2Division of Rheumatology, Department of Internal Medicine, Seoul National University Hospital, Seoul, Korea, Republic of

Abstract

Background Mast cells (MCs) function as immune sentinel cells in the tissue. The well-known cellular infiltrate in inflammatory myositis mainly consists of macrophages and lymphocytes that produce numerous inflammatory cytokines and chemokines augmenting inflammatory cell infiltration and damage of myofibers. The role of tissue-resident MCs has not been well studied in inflammatory myositis.

Objectives To study the phenotype and role of MCs in a murine myositis model.

Methods C-protein induced myositis (CIM) was induced with human skeletal C-protein fragment in 8 week-old female MC-deficient SASH mice and C57BL/6 controls. Quadriceps muscles of both legs were harvested at day 21. Toluidine blue stain was used to identify degranulating MCs in the muscle tissue. Immunohistochemistry was performed to detect mouse mast cell protease (mMCP)-1, -4, -5, -6 positive MCs.

Results MCs were mainly located in the connective tissue between fascicles showing a connective tissue MC phenotype. The density of MCs and percentage of degranulating MCs per 5 high power field (HPF) were increased in CIM tissues (Figure). MC deficient mice had lower histology score of muscle inflammation compared with controls. The difference mainly attributed to abrogated invasiveness of inflammatory infiltrates into fascicles in MC deficient mice.

Conclusions Connective tissue-type MCs in skeletal muscles are activated upon CIM induction. MCs facilitate tissue invasion of inflammatory infiltrates into muscles in the CIM model.

Acknowledgements We would like to thank Dr. Hitoshi Kohsaka for providing the C-protein construct and helpful discussions regarding this study. We also thank Dr. Michael Gurish for the antibodies.

Disclosure of Interest None Declared

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