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ABSTRACT: Background
The idiopathic inflammatory myopathies represent a group of autoimmune diseases that are characterized by lymphocyte infiltration of muscle and muscle weakness. Insulin-like 6 (Insl6) is a poorly characterized member of the insulin-like/relaxin family of secreted proteins, whose expression is upregulated upon acute muscle injury.Methods
In this study, we employed Insl6 gain or loss of function mice to investigate the role of Insl6 in a T cell-mediated model of experimental autoimmune myositis (EAM). EAM models in rodents have involved immunization with human myosin-binding protein C with complete Freund's adjuvant (CFA) emulsions and pertussis toxin.Results
Insl6-deficiency in mice led to a worsened myositis phenotype including increased infiltration of C
SUBMITTER: Zeng L
PROVIDER: S-EPMC4144317 | biostudies-literature | 2014
REPOSITORIES: biostudies-literature