Icos gene disruption in non-obese diabetic mice elicits myositis associated with anti-troponin T3 autoantibodies.
ICOS
NOD
TNNT3
autoantibody
idiopathic inflammatory myopathies (IIM)
mouse
myositis
Journal
Neuropathology and applied neurobiology
ISSN: 1365-2990
Titre abrégé: Neuropathol Appl Neurobiol
Pays: England
ID NLM: 7609829
Informations de publication
Date de publication:
02 2023
02 2023
Historique:
revised:
01
02
2023
received:
21
06
2022
accepted:
05
02
2023
pubmed:
9
2
2023
medline:
3
3
2023
entrez:
8
2
2023
Statut:
ppublish
Résumé
Idiopathic inflammatory myopathies (IIM) are autoimmune inflammatory disorders leading to skeletal muscle weakness and disability. The pathophysiology of IIM is poorly understood due to the scarcity of animal disease models. Genetic deletion of Icos or Icosl (inducible T cell co-stimulator/ligand) in non-obese diabetic (NOD) mice leads to muscle disease. Our aim was to characterise Icos Diabetes, weight, myopathy incidence/clinical score and grip strength were assessed over time. Locomotor activity was analysed with the Catwalk XT gait analysis system. Muscle histology was evaluated in haematoxylin/eosin and Sirius red-stained sections, and immune infiltrates were characterised by immunofluorescence and flow cytometry. 2D gel electrophoresis of muscle protein extracts and mass spectrometry were used to identify novel aAbs. NOD mice were immunised with troponin T3 (TNNT3) in incomplete Freund's adjuvant (IFA) and R848. An addressable laser bead immunoassay (ALBIA) was developed to measure aAb IgG serum levels. Icos These data show that Icos
Substances chimiques
Autoantibodies
0
Troponin T
0
Icos protein, mouse
0
Inducible T-Cell Co-Stimulator Protein
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e12889Informations de copyright
© 2023 The Authors. Neuropathology and Applied Neurobiology published by John Wiley & Sons Ltd on behalf of British Neuropathological Society.
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