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dc.contributor.authorWen, Li
dc.contributor.authorGreen, E. Allison
dc.contributor.authorStratmann, Thomas
dc.contributor.authorPanosa, Anaïs
dc.contributor.authorGomis, Ramon
dc.contributor.authorEynon, Elizabeth E.
dc.contributor.authorFlavell, Richard A.
dc.contributor.authorMezquita, Jovita A.
dc.contributor.authorMora Giral, Concepció
dc.date.accessioned2021-04-22T09:03:41Z
dc.date.available2021-04-22T09:03:41Z
dc.date.issued2011
dc.identifier.issn0014-2980 (paper)
dc.identifier.issn0014-2980 (electrònic)
dc.identifier.urihttp://hdl.handle.net/10459.1/71127
dc.description.abstractCD4+ T lymphocytes are required to induce spontaneous autoimmune diabetes in the NOD (Non Obese Diabetic) mouse. Since pancreatic β cells upregulate Fas expression upon exposure to proinflammatory cytokines, we studied whether the diabetogenic action of CD4+ T lymphocytes depends on Fas expression on target cells. We assayed the diabetogenic capacity of NOD spleen CD4+ T lymphocytes when adoptively transferred into a NOD mouse model combining: a) Fas-deficiency, b) FasL-deficiency, and c) the SCID mutation. We found that CD4+ T lymphocytes require Fas expression in the recipients’ target cells to induce diabetes. IL-1β has been described as a key cytokine involved in Fas up-regulation on mouse β cells. We addressed whether CD4+ T cells require IL-1β to induce diabetes. We also studied spontaneous diabetes onset in NOD/ICE (Interleukin-1 Converting Enzyme) deficient mice, in NOD/IL-1β deficient mice, and CD4+ T cell-adoptively transferred diabetes into NOD/SCID IL-1β-deficient mice. Neither IL-1β nor IL-18 are required for either spontaneous or CD4+ T-cell adoptively transferred diabetes. We conclude that CD4+ T cell-mediated β cell damage in autoimmune diabetes depends on Fas expression, but not on IL-1β, unveiling the existing redundancy regarding the cytokines involved in Fas upregulation on NOD β cells in vivo.ca_ES
dc.description.sponsorshipThis work was supported by the Juvenile Diabetes Research Foundation Advanced Post‐doctoral Fellowship ref. 10‐2000‐635 (to C.M.), the Spanish Ministerio de Sanidad y Consumo ISCIII (ref. 01/3127) (to C.M.), and Ministerio de Ciencia y Tecnología Grants SAF 2003‐06139, SAF2006‐07757 (to C.M.), the Juvenile Diabetes Research Foundation Career Development Award 298210 and NIH/NIAID RO1 AI‐44427 (to L.W.), the Ministry of Science and Technology SAF 2003‐06018 (to R.G.), the NIH P30 DK45735 and R01 DK/AI51665 (to R.A.F.). R.A.F. is an investigator of the Howard Hughes Medical Institute. C.M. investigator in the University of Lleida/IRB Lleida investigator (Institut d'Investigacions Biomèdiques Lleida), We would like to thank Lex van der Ploeg (Merck Research Laboratories) for providing us with the IL‐1β‐deficient mice on the B10.RIII (H2<r>(71NS)/Sn) genetic background; Jose Luis Navarro, Isabel Crespo, Marta Julià, Sílvia Moreno, and Ainhoa García for technical assistance; Emma Arcos and Llorenç Quintó for statistical analysis; and Frances Manzo for her assistance with manuscript preparation.ca_ES
dc.language.isoengca_ES
dc.publisherWileyca_ES
dc.relationMIECI/PN2004-2007/SAF2006‐0775ca_ES
dc.relationMICYT/PN2000-2003/SAF2003‐06139ca_ES
dc.relationMICYT/PN2000-2003/SAF2003‐06018ca_ES
dc.relation.isformatofVesió postprint del document publicat a https://doi.org/10.1002/eji.201041216ca_ES
dc.relation.ispartofEuropean Journal of Immunology, 2011, vol. 41, núm. 5, p. 1344-51ca_ES
dc.rights(c) Wiley, 2011ca_ES
dc.subjectAutoimmune diabetesca_ES
dc.subjectβ cell apoptosisca_ES
dc.subjectFasca_ES
dc.subjectCD4+ T cellsca_ES
dc.titleIn vivo diabetogenic action of CD41+ T lymphocytes requires Fas expression and is independent of IL-1 and IL-18ca_ES
dc.typeinfo:eu-repo/semantics/articleca_ES
dc.identifier.idgrec016580
dc.type.versioninfo:eu-repo/semantics/acceptedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.1002/eji.201041216


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