Smad7 in intestinal CD4
Animals
Autoimmunity
/ physiology
CD4-Positive T-Lymphocytes
/ immunology
Cell Differentiation
Central Nervous System
/ metabolism
Disease Models, Animal
Encephalomyelitis
/ metabolism
Encephalomyelitis, Autoimmune, Experimental
/ immunology
Gastrointestinal Microbiome
/ physiology
Gene Expression Regulation
Humans
Immune Tolerance
Inflammation
Intestines
/ pathology
Mice
Mice, Transgenic
Multiple Sclerosis
/ metabolism
Signal Transduction
Smad7 Protein
/ genetics
Spinal Cord
/ pathology
Transforming Growth Factor beta
/ metabolism
Smad7
T helper cell
TGF-beta
gut–brain axis
multiple sclerosis
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
17 12 2019
17 12 2019
Historique:
pubmed:
5
12
2019
medline:
2
4
2020
entrez:
5
12
2019
Statut:
ppublish
Résumé
Environmental triggers acting at the intestinal barrier are thought to contribute to the initiation of autoimmune disorders. The transforming growth factor beta inhibitor Smad7 determines the phenotype of CD4
Identifiants
pubmed: 31796589
pii: 1905955116
doi: 10.1073/pnas.1905955116
pmc: PMC6926056
doi:
Substances chimiques
SMAD7 protein, human
0
Smad7 Protein
0
Smad7 protein, mouse
0
Transforming Growth Factor beta
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
25860-25869Déclaration de conflit d'intérêts
Competing interest statement: S.C.J. received travel funding and/or speaker honoraria from Bayer, Novartis, and Roche; and received research support from Bayer, Novartis, Roche, and Ursapharm; all unrelated to the content of this manuscript. T.B. received speaker honoraria from Biogen, Novartis, and Roche; and is a member of the advisory board for Immunology of Novartis; all unrelated to the content of this manuscript. R.G. received speaker and board honoraria from Baxter, Bayer Schering, Biogen Idec, CLB Behring, Genzyme, Merck Serono, Novartis, Stendhal, Talecris, and TEVA; and his department received grant support from Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, and TEVA; all unrelated to the content of this manuscript. S.F. received travel grants from Biogen Idec and Genzyme; speaker or board honoraria from Novartis and Celgene; and research support from Novartis; all unrelated to the content of this manuscript. I.K. has received speaker honoraria and travel funding from Bayer, Biogen, Novartis, Merck, Sanofi Genzyme, and Roche; speaker honoraria from Mylan; travel funding from the Guthy-Jackson Charitable Foundation; consulted for Alexion, Bayer, Biogen, Chugai, IQVIA, Novartis, Merck, and Roche; and received research support from Chugai and Diamed; all unrelated to the content of this manuscript.
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