Zobrazeno 1 - 10
of 44
pro vyhledávání: '"Ute Christine Rogner"'
Autor:
Louis Pérol, John M. Lindner, Pamela Caudana, Nicolas Gonzalo Nunez, Audrey Baeyens, Andrea Valle, Christine Sedlik, Delphine Loirat, Olivier Boyer, Alain Créange, José Laurent Cohen, Ute Christine Rogner, Jun Yamanouchi, Martine Marchant, Xavier Charles Leber, Meike Scharenberg, Marie-Claude Gagnerault, Roberto Mallone, Manuela Battaglia, Pere Santamaria, Agnès Hartemann, Elisabetta Traggiai, Eliane Piaggio
Publikováno v:
Nature Communications, Vol 7, Iss 1, Pp 1-10 (2016)
Type 1 diabetes is driven by T-cell autoimmunity to pancreatic islet cells. Here the authors show that autoreactive anti-IL-2 T and B cells are present in type 1 diabetes patients, and that anti-IL-2 antibodies precede diabetes onset in mice, suggest
Externí odkaz:
https://doaj.org/article/db770a8739b84dbf870ffd96cace147e
Autor:
Philippe J. Sansonetti, Matthieu Rouland, Maria Rescigno, Lucie Cagninacci, Nathalie Vergnolle, Sandra Guilmeau, Juliette Mouriès, Latif Rachdi, Lucie Beaudoin, Azadeh Saffarian, Agnès Lehuen, Dalale Gueddouri, Anne-Françoise Burnol, Ute Christine Rogner, Asmaa Tazi, Ophélie Rouxel, Léo Bertrand, Thierry Pedron
Publikováno v:
Gut
Gut, BMJ Publishing Group, 2021, pp.gutjnl-2020-323664. ⟨10.1136/gutjnl-2020-323664⟩
Gut, 2022, 71 (2), pp.296-308. ⟨10.1136/gutjnl-2020-323664⟩
Gut, BMJ Publishing Group, 2022, 71 (2), pp.296-308. ⟨10.1136/gutjnl-2020-323664⟩
Gut, BMJ Publishing Group, 2021, pp.gutjnl-2020-323664. ⟨10.1136/gutjnl-2020-323664⟩
Gut, 2022, 71 (2), pp.296-308. ⟨10.1136/gutjnl-2020-323664⟩
Gut, BMJ Publishing Group, 2022, 71 (2), pp.296-308. ⟨10.1136/gutjnl-2020-323664⟩
ObjectiveType 1 diabetes (T1D) is an autoimmune disease caused by the destruction of pancreatic β-cells producing insulin. Both T1D patients and animal models exhibit gut microbiota and mucosa alterations, although the exact cause for these remains
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1fb48f2c56af7d5c4cecd81eea64b65c
https://hal.archives-ouvertes.fr/hal-03432361
https://hal.archives-ouvertes.fr/hal-03432361
Publikováno v:
Mammalian Genome
Mammalian Genome, 2017, 28 (1-2), pp.1-12. ⟨10.1007/s00335-016-9665-4⟩
Mammalian Genome, Springer Verlag, 2017, 28 (1-2), pp.1-12. ⟨10.1007/s00335-016-9665-4⟩
Mammalian Genome, 2017, 28 (1-2), pp.1-12. ⟨10.1007/s00335-016-9665-4⟩
Mammalian Genome, Springer Verlag, 2017, 28 (1-2), pp.1-12. ⟨10.1007/s00335-016-9665-4⟩
Nonobese diabetic (NOD) mice are a model for type 1 diabetes that displays defects in central immune tolerance, including impairment of thymocyte apoptosis and proliferation. Thymocyte apoptosis is decreased in NOD/Lt mice compared to nondiabetic C3H
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::cf6e2b8565b42dbc5cb2bd8059cf4820
https://hal.science/hal-03051465/document
https://hal.science/hal-03051465/document
Autor:
Roberto Mallone, Louis Pérol, Marie Claude Gagnerault, Alain Créange, Jun Yamanouchi, Meike Scharenberg, Pere Santamaria, Audrey Baeyens, Agnès Hartemann, José L. Cohen, Ute Christine Rogner, Olivier Boyer, Martine Marchant, Delphine Loirat, Elisabetta Traggiai, Christine Sedlik, Nicolás Gonzalo Núñez, Andrea Valle, Manuela Battaglia, Pamela Caudana, Eliane Piaggio, John M. Lindner, Xavier Charles Leber
Publikováno v:
Nature Communications
Nature Communications, Nature Publishing Group, 2016, 7 (1), ⟨10.1038/ncomms13027⟩
Nature Communications, 2016, 7 (1), ⟨10.1038/ncomms13027⟩
Nature Communications, Vol 7, Iss 1, Pp 1-10 (2016)
Nature Communications, Nature Publishing Group, 2016, 7 (1), ⟨10.1038/ncomms13027⟩
Nature Communications, 2016, 7 (1), ⟨10.1038/ncomms13027⟩
Nature Communications, Vol 7, Iss 1, Pp 1-10 (2016)
Type 1 diabetes (T1D) is characterized by a chronic, progressive autoimmune attack against pancreas-specific antigens, effecting the destruction of insulin-producing β-cells. Here we show interleukin-2 (IL-2) is a non-pancreatic autoimmune target in
Publikováno v:
Clinical and Experimental Pharmacology and Physiology. 37:1154-1158
Summary 1. Our previous studies of the murine genetic locus Idd6 revealed the aryl hydrocarbon receptor nuclear translocator-like protein 2 (Arntl2) as a candidate gene for type 1 diabetes; and in Idd6 NOD.C3H congenic mice, Arntl2 upregulation is li
Publikováno v:
Immunogenetics. 62:585-592
The genetic locus Idd6 is involved in type 1 diabetes development in the non-obese diabetic (NOD) mouse through its effect on the immune system and in particular, on T cell activities. Analysis of congenic strains for Idd6 has established the Aryl hy
Autor:
Angelita Rebollo, Patrice Debré, Katy Billot, Dominique Mazier, Issam Arrouss, Christophe Parizot, Ute Christine Rogner
Publikováno v:
Leukemia Research. 34:289-293
The Aiolos transcription factor plays a crucial role in the control of lymphocyte differentiation and proliferation. The expression of Aiolos isoform has been studied in lymphoid pathologies but nothing is known about its expression in unaffected hum
Publikováno v:
The Journal of Immunology. 179:3896-3903
The Idd6 locus on mouse chromosome 6, which controls the development of type 1 diabetes in the NOD mouse, affects proliferation rates of T cells and the activity of regulatory CD4+CD25+ T cells. Using a transcriptional profiling approach, we show tha
Publikováno v:
Molecular and Cellular Biology. 27:6093-6102
The deletion of the neuronal Nap1l2 (nucleosome assembly protein 1-like 2) gene in mice causes neural tube defects. We demonstrate here that this phenotype correlates with deficiencies in differentiation and increased maintenance of the neural stem c
Publikováno v:
Human Molecular Genetics. 15:2732-2742
The Idd6 murine type 1 diabetes locus has been shown to control diabetes by regulating the protective activity of the peripheral immune system, as demonstrated by diabetes transfer assays using splenocytes. The analysis of three novel subcongenic (NO