4.5 Article

Leptin Promoted IL-17 Production from ILC2s in Allergic Rhinitis

Journal

MEDIATORS OF INFLAMMATION
Volume 2020, Issue -, Pages -

Publisher

HINDAWI LTD
DOI: 10.1155/2020/9248479

Keywords

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Funding

  1. National Natural Science Grant of China [81600785, 81700892, 81970861]
  2. Pearl River S and T Nova Program of Guangzhou [201710010085]
  3. Key Clinical Specialty of Guangzhou Women and Children's Medical Center
  4. Institute of Pediatrics of Guangzhou Women and Children's Medical Center [YIP-2016-022, Pre-NSFC-2018-005]
  5. Dongguan Social Science and Technology Development (Key) Project [201950715024194]
  6. Guangdong Province Natural Science Grant [2016A03031016]

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Background. Interleukin-17 plays important roles in allergic diseases. Several studies proved that leptin promoted Th17 immune responses by inducing ROR gamma t transcription. ILC2 is an important member of the early stage of immune response. Therefore, we aimed to explore the effect of leptin on the IL-17 production by ILC2 in AR in this study.Methods. Fifteen AR patients and fifteen healthy controls were enrolled. Serum leptin levels were measured, and their correlation with the frequency of IL-17+ ILC2 cells was analyzed using enzyme-linked immunosorbent assay (ELISA) and flow cytometry. ILC2 was stimulated by leptin, and the expression of IL-17, IL-5, and IL-13 was detected by ELISA. The correlated pathways were confirmed by real-time PCR.Results. We found that serum leptin and the frequency of IL-17-producing ILC2s in AR were significantly higher compared with those in controls. After being incubated with leptin, the frequency of IL-17+ ILC2 cells and IL-17 production from ILC2 was upregulated compared with that in controls. We also found that leptin induced ROR gamma t and Ahr expression by ILC2. Moreover, leptin-induced IL-17-producing ILC2 concomitantly expressed IL-5 and IL-13.Conclusions. Our data provide preliminary evidence that leptin-induced IL-17 production from ILC2 cells is dependent on ROR gamma t and Ahr expression and the blockade of leptin may be a promising target for the treatment of AR.

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