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首页> 外文期刊>Cell and Tissue Research >Th22 cells induce Muller cell activation via the Act1/TRAF6 pathway in diabetic retinopathy
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Th22 cells induce Muller cell activation via the Act1/TRAF6 pathway in diabetic retinopathy

机译：Th22 cells induce Muller cell activation via the Act1/TRAF6 pathway in diabetic retinopathy

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T helper 22 (Th22) cells have been implicated in diabetic retinopathy (DR), but it remains unclear whether Th22 cells involve in the pathogenesis of DR. To investigate the role of Th22 cells in DR mice, the animal models were established by intraperitoneal injection of STZ and confirmed by fundus fluorescein angiography and retinal haematoxylin-eosin staining. IL-22BP was administered by intravitreal injection. IL-22 level was measured by ELISA in vivo and in vitro. The expression of IL-22R alpha 1 in the retina was assessed by immunofluorescence. We assessed GFAP, VEGF, ICAM-1, inflammatory-associated factors and the integrity of blood-retinal barrier in control, DR, IL-22BP, and sham group. Muller cells were co-cultured with Th22 cells, and the expression of the above proteins was measured by immunoblotting. Plasmid transfection technique was used to silence Act1 gene in Muller cells. Results in vivo and in vitro indicated that Th22 cells infiltrated into the DR retinal and IL-22R alpha 1 expressed in Muller cells. Th22 cells promoted Muller cells activation and inflammatory factor secretion by secreting IL-22 compared with high-glucose stimulation alone. In addition, IL-22BP ameliorated the pathological alterations of the retina in DR. Inhibition of the inflammatory signalling cascade through Act1 knockdown alleviated DR-like pathology. All in all, the results suggested that Th22 cells infiltrated into the retina and secreted IL-22 in DR, and then IL-22 binding with IL-22R alpha 1 activated the Act1/TRAF6 signal pathway, and promoted the inflammatory of Muller cells and involved the pathogenesis of DR.

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