Cutting edge: Leptin-induced RORγt expression in CD4+ T cells promotes Th17 responses in systemic lupus erythematosus

Yiyun Yu, Yaoyang Liu, Fu Dong Shi, Hejian Zou, Giuseppe Matarese, Antonio La Cava

Research output: Contribution to journalArticle

Abstract

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 RORgt transcription. Leptin also increased Th17 responses in (NZB 3 NZW)F1 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.

Original languageEnglish
Pages (from-to)3054-3058
Number of pages5
JournalJournal of Immunology
Volume190
Issue number7
DOIs
Publication statusPublished - Apr 1 2013

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ASJC Scopus subject areas

  • Immunology

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