替妥木单抗治疗甲状腺相关性眼病的机制OA

Objective To explore the effect of the insulin-like growth factor I receptor(IGF-IR)inhibitor telumumab on the expression of MHC-Ⅱand B7 co-stimulatory molecules(CD80,CD86,PD-L1)on the surface of CD34+fibroblasts in patients with thyroid-associated ophthalmopathy(TAO),and to explore its potential therapeutic mechanism.Methods Peripheral blood samples of TAO patients were collected,CD34+fibroblasts were isolated and differentiated.The differentiated CD34+fibroblasts were randomly divided into two groups.The Teplizumab group was added with teplizumab(final concentration 50 μg/ml),while the CD34+cells of TAO patients in the control group were not cultured with any drugs.Normal human CD34+cells were cultured as the normal group.The expression changes of MHC-Ⅱ,CD80,CD86 and PD-L1 on the surface of CD34+fibroblasts in the three groups were compared.Results Compared with the normal group,the levels of MHC-Ⅱ,CD80,CD86 and PD-LI in CD34+fibroblasts of the control group were significantly increased(P＜0.05);Compared with the control group,the levels of MHC-Ⅱ,CD80,CD86 and PD-LI in CD34+fibroblasts in the tipromab group were significantly decreased(P＜0.05).Conclusion Tintumab provides a theoretical basis for the targeted therapy of TAO by inhibiting the IGF-IR signaling pathway and down-regulating the expression of antigen presentation and co-stimulatory molecules.