Abstract
SummaryMacrophages are involved in low‐grade inflammation in diabetes, and play pathogenic roles in proliferative diabetic retinopathy (PDR) by producing proinflammatory cytokines. T cells as well as other cells are activated by proinflammatory cytokines, and the infiltration into the vitreous of patients with PDR has been shown. We have recently found that both positive rates and levels of IL4, IL‐6, IL‐10, IL‐17A, IL‐21, IL‐22, and TNFα in the vitreous of PDR patients were significantly higher than those in the serum, and that vitreous levels of these cytokines and IL‐31 were significantly higher in PDR patients than in epiretinal membrane or macular hole patients. In addition, although vitreous of IFN‐g and sCD40L in the vitreous of endogenous uveitis (EU) patients were significantly higher than those of PDR patients, vitreous levels of IL‐4, IL‐17A, IL‐22, IL‐31, and TNFa were conversely higher in the vitreous of PDR patients than those of EU patients. Although it is unclear whether these cytokines synergistically play facilitative roles or inhibitory roles for the progression of PDR, our study suggested that Th2‐ and Th17‐related immune responses are involved in the pathogenesis of PDR.
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