Journal
BIOENGINEERED
Volume 13, Issue 5, Pages 13293-13299Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/21655979.2022.2080367
Keywords
IL-35; IL-17; Th17 cell; ROR alpha; ROR gamma t; proliferative diabetic retinopathy
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Funding
- Zunyi Science and Technology Bureau Joint Research and Development Fund Project [(2017)35]
- National Nature Science Foundation of China [82160200]
- R&D Program of The First People's Hospital of Zunyi [2020)4]
- Science and Technology Fund Project of Guizhou Provincial Health Commission [gzwjk2020-1-155]
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IL-35 protects against proliferative diabetic retinopathy by reducing IL-17 levels and inhibiting Th17 cell differentiation.
T helper 17 (Th17) cells regulate inflammatory processes and are implicated in pathogenesis of proliferative diabetic retinopathy (PDR) through modulation of interleukin-17 (IL-17). IL-35, anti-inflammatory factor, negatively mediates IL-17 expression and Th17 differentiation. In this study, the role of IL-35 in PDR was assessed. The results showed that IL-35 was down-regulated, while IL-17 was up-regulated, in peripheral blood mononuclear cells (PBMCs) of PDR patients. In addition, immunofluorescence analysis indicated that frequency of Th17 cells was enhanced in the PBMCs of PDR patients. However, incubation with IL-35 reduced the Th17 cell frequency and decreased the level of IL-17 in CD4(+) T lymphocytes. Moreover, the levels of transcription factors essential for Th17 differentiation, ROR alpha (retinoid-related orphan receptor alpha) and ROR gamma t, were reduced by IL-35 treatment. In conclusion, IL-35 reduced level of IL-17 and inhibited Th17 differentiation to protect against PDR. [GRAPHICS] .
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