Journal
JOURNAL OF IMMUNOLOGY
Volume 190, Issue 7, Pages 3054-3058Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1203275
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Funding
- National Institutes of Health [AR53239, AI95921, AI83294]
- European Union Ideas Programme, European Research Council Starting Grant [310496]
- Telethon/Juvenile Diabetes Research Foundation [GJT08004]
- Fondo per Gli Investimenti Della Ricerca di Base Merit Grant [RBNE08HWLZ]
- Fondazione Telethon Funding Source: Custom
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Th17 CD4(+) cells promote inflammation and autoimmunity. In this study, we report that Th17 cell frequency is reduced in ob/ob mice (that are genetically deficient in the adipokine leptin) and that the administration of leptin to ob/ob mice restored Th17 cell numbers to values comparable to those found in wildtype animals. Leptin promoted Th17 responses in normal human CD4(+) T cells and in mice, both in vitro and in vivo, by inducing ROR gamma t transcription. Leptin also increased Th17 responses in (NZB x NZW) F-1 lupus-prone mice, whereas its neutralization in those autoimmune-prone mice inhibited Th17 responses. Because Th17 cells play an important role in the development and maintenance of inflammation and autoimmunity, these findings envision the possibility to modulate abnormal Th17 responses via leptin manipulation, and they reiterate the link between metabolism/nutrition and susceptibility to autoimmunity. The Journal of Immunology, 2013, 190: 3054-3058.
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