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Med Sci (Paris). 2018 Nov;34 Hors série n°2:35-38. doi: 10.1051/medsci/201834s210. Epub 2018 Nov 12.

[The effect of interferon-gamma on skeletal muscle cell biology].

[Article in French]

Author information

1
ED402, Paris Est-Créteil University, Créteil, France - Inserm U955 Team 10, Paris Est-Créteil University, Créteil, France.
2
Inserm U955 Team 10, Paris Est-Créteil University, Créteil, France.

Abstract

Dysimmune and inflammatory myopathies (DIMs) affect around 14/100,000 people worldwide. Based on immupour nopathological criteria, DIMs are divided in four groups: (1) polymyositis (PM)/inclusion body myositis (IBM), (2) dermatomyositis (DM), (3) immune-mediated necrotizing myopathies (IMNM) and (iv) overlapping myositis including anti-synthetase syndrome (ASS). ASS and PM/IBM are characterized by the activation of inflammation with lymphocytic infiltrations. Recently, we showed that an expression of the major histocompatibility complex class 2 (MHC2) was present in myofibers from ASS and IBM muscle biopsies. Interestingly, MHC2 expression is known to be stimulated by Interferon-gamma (IFNγ) in myogenic cells. LTCD8 cells, which are well-known producers of IFNγ, are commonly found in close vicinity to MHC2 positive myofibers. This inflammatory cytokine also inhibits myogenic differentiation in vitro by CIITA-myogenin interaction. The mechanisms involved in the lymphocyte-driven muscle toxicity in DIMs are unclear. The objectives of this project are to characterize IFNγ effects on the biology of human myogenic cells by morphological, molecular and cellular approaches. Then, we aim to investigate the role of IFNγ in these myopathies and its impact during muscular regeneration. In vitro preliminary studies have been performed using human and mouse myoblasts treated or not with IFNγ. Our results should lead to a better understanding of the role of IFNγ in the pathophysiology of DIMs, and would hopefully help identify new therapeutic targets.

PMID:
30418144
DOI:
10.1051/medsci/201834s210

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