Leptin Modulates the Survival of Autoreactive CD4+ T Cells through the Nutrient/Energy-Sensing Mammalian Target of Rapamycin Signaling Pathway. (Articolo in rivista)

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  • Leptin Modulates the Survival of Autoreactive CD4+ T Cells through the Nutrient/Energy-Sensing Mammalian Target of Rapamycin Signaling Pathway. (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Alternative label
  • Galgani M; Procaccini C; De Rosa V; Carbone F; Chieffi P; La Cava A; Matarese G. (2010)
    Leptin Modulates the Survival of Autoreactive CD4+ T Cells through the Nutrient/Energy-Sensing Mammalian Target of Rapamycin Signaling Pathway.
    in The Journal of immunology (1950)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Galgani M; Procaccini C; De Rosa V; Carbone F; Chieffi P; La Cava A; Matarese G. (literal)
Pagina inizio
  • 7474 (literal)
Pagina fine
  • 7479 (literal)
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  • 15 (literal)
Rivista
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  • 6 (literal)
Note
  • ISI Web of Science (WOS) (literal)
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  • *Laboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale delle Ricerche; +Laboratorio di Immunologia, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Universita` di Napoli \"Federico II\"; ?Dipartimento di Medicina Sperimentale, II Universita` di Napoli, Napoli, Italy; and xDepartment of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095 (literal)
Titolo
  • Leptin Modulates the Survival of Autoreactive CD4+ T Cells through the Nutrient/Energy-Sensing Mammalian Target of Rapamycin Signaling Pathway. (literal)
Abstract
  • Chronic inflammation can associate with autoreactive immune responses, including CD4(+) T cell responses to self-Ags. In this paper, we show that the adipocyte-derived proinflammatory hormone leptin can affect the survival and proliferation of autoreactive CD4(+) T cells in experimental autoimmune encephalomyelitis, an animal model of human multiple sclerosis. We found that myelin olygodendrocyte glycoprotein peptide 35-55 (MOG(35-55))-specific CD4(+) T cells from C57BL/6J wild-type mice could not transfer experimental autoimmune encephalomyelitis into leptin-deficient ob/ob mice. Such a finding was associated with a reduced proliferation of the transferred MOG(35-55)-reactive CD4(+) T cells, which had a reduced degradation of the cyclin-dependent kinase inhibitor p27(kip1) and ERK1/2 phosphorylation. The transferred cells displayed reduced Th1/Th17 responses and reduced delayed-type hypersensitivity. Moreover, MOG(35-55)-reactive CD4(+) T cells in ob/ob mice underwent apoptosis that associated with a downmodulation of Bcl-2. Similar results were observed in transgenic AND-TCR- mice carrying a TCR specific for the pigeon cytochrome c 88-104 peptide. These molecular events reveal a reduced activity of the nutrient/energy-sensing AKT/mammalian target of rapamycin pathway, which can be restored in vivo by exogenous leptin replacement. These results may help to explain a link between chronic inflammation and autoimmune T cell reactivity. (literal)
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