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- Publisher Website: 10.1002/eji.201040416
- Scopus: eid_2-s2.0-77956096397
- PMID: 20544729
- WOS: WOS:000281305900026
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Article: Abrogation of ICOS/ICOS ligand costimulation in NOD mice results in autoimmune deviation toward the neuromuscular system
Title | Abrogation of ICOS/ICOS ligand costimulation in NOD mice results in autoimmune deviation toward the neuromuscular system |
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Authors | |
Keywords | ICOS ligand Costimulation ICOS Autoimmunity Type 1 diabetes |
Issue Date | 2010 |
Citation | European Journal of Immunology, 2010, v. 40, n. 8, p. 2267-2276 How to Cite? |
Abstract | NOD mice spontaneously develop insulin-dependent diabetes around 10-40wk of age. Numerous immune gene variants contribute to the autoimmune process. However, genes that direct the autoimmune response toward β cells remain ill defined. In this study, we provide evidence that the Icos and Icosl genes contribute to the diabetes process. Protection from diabetes in ICOS -/- and ICOSL-/- NOD mice was unexpectedly associated with the development of an autoimmune disorder of the neuro-muscular system, characterized by myositis, sensory ganglionitis and, to a reduced extent, inflammatory infiltrates in the CNS. This syndrome was reproduced upon adoptive transfer of CD4+ and CD8+ T cells from diseased donors to naïve NOD.scid recipients. Our data further show that protection from diabetes results from defective activation of autoimmune diabetogenic effector T cells in ICOS-/- NOD mice, whereas acceleration of diabetes in BDC2.5 ICOS-/- NOD mice is induced by a dominant defect in Treg. Taken together, our findings indicate that costimulation signals play a key role in regulating immune tolerance in peripheral tissues and that the ICOS/ICOSL costimulatory pathway influences the balance between Treg and diabetogenic effector T cells. © 2010 Wiley-VCH Verlag GmbH & Co. KGaA. |
Persistent Identifier | http://hdl.handle.net/10722/291984 |
ISSN | 2023 Impact Factor: 4.5 2023 SCImago Journal Rankings: 1.627 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Prevot, Nicolas | - |
dc.contributor.author | Briet, Claire | - |
dc.contributor.author | Lassmann, Hans | - |
dc.contributor.author | Tardivel, Isabelle | - |
dc.contributor.author | Roy, Edwige | - |
dc.contributor.author | Morin, Joëlle | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Tafuri, Anna | - |
dc.contributor.author | Boitard, Christian | - |
dc.date.accessioned | 2020-11-17T14:55:31Z | - |
dc.date.available | 2020-11-17T14:55:31Z | - |
dc.date.issued | 2010 | - |
dc.identifier.citation | European Journal of Immunology, 2010, v. 40, n. 8, p. 2267-2276 | - |
dc.identifier.issn | 0014-2980 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291984 | - |
dc.description.abstract | NOD mice spontaneously develop insulin-dependent diabetes around 10-40wk of age. Numerous immune gene variants contribute to the autoimmune process. However, genes that direct the autoimmune response toward β cells remain ill defined. In this study, we provide evidence that the Icos and Icosl genes contribute to the diabetes process. Protection from diabetes in ICOS -/- and ICOSL-/- NOD mice was unexpectedly associated with the development of an autoimmune disorder of the neuro-muscular system, characterized by myositis, sensory ganglionitis and, to a reduced extent, inflammatory infiltrates in the CNS. This syndrome was reproduced upon adoptive transfer of CD4+ and CD8+ T cells from diseased donors to naïve NOD.scid recipients. Our data further show that protection from diabetes results from defective activation of autoimmune diabetogenic effector T cells in ICOS-/- NOD mice, whereas acceleration of diabetes in BDC2.5 ICOS-/- NOD mice is induced by a dominant defect in Treg. Taken together, our findings indicate that costimulation signals play a key role in regulating immune tolerance in peripheral tissues and that the ICOS/ICOSL costimulatory pathway influences the balance between Treg and diabetogenic effector T cells. © 2010 Wiley-VCH Verlag GmbH & Co. KGaA. | - |
dc.language | eng | - |
dc.relation.ispartof | European Journal of Immunology | - |
dc.subject | ICOS ligand | - |
dc.subject | Costimulation | - |
dc.subject | ICOS | - |
dc.subject | Autoimmunity | - |
dc.subject | Type 1 diabetes | - |
dc.title | Abrogation of ICOS/ICOS ligand costimulation in NOD mice results in autoimmune deviation toward the neuromuscular system | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1002/eji.201040416 | - |
dc.identifier.pmid | 20544729 | - |
dc.identifier.scopus | eid_2-s2.0-77956096397 | - |
dc.identifier.volume | 40 | - |
dc.identifier.issue | 8 | - |
dc.identifier.spage | 2267 | - |
dc.identifier.epage | 2276 | - |
dc.identifier.eissn | 1521-4141 | - |
dc.identifier.isi | WOS:000281305900026 | - |
dc.identifier.issnl | 0014-2980 | - |