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目的探讨CD3~+CD56~+自然杀伤T细胞(natural killer T cell,NKT)及其分泌的白细胞介素(interleukin,IL)-2、IL-6、IL-10、IL-12、肿瘤坏死因子-α(tumor necrosis factor-alpha,TNF-α)等细胞因子和血清游离三碘甲状腺原氨酸(free triiodothyronine,FT_3)、游离甲状腺素(free thyroxine,FT_4)、促甲状腺激素(thyroid stimulating hormone,TSH)、甲状腺过氧化物酶抗体(thyroid peroxidase antibody,TPOAb)、甲状腺球蛋白抗体(thyroglobulin antibody,TGAb)和促甲状腺素受体抗体(thyrotrophin receptor antibody,TRAb)水平在Graves病患者体内表达情况。方法 Graves病患者30例为观察组,同期体检健康者30例为对照组,检测2组外周血CD3~+CD56~+NKT占淋巴细胞比率、CD3~+CD56~+NKT分泌的细胞因子IL-2、IL-6、IL-10、IL-12、TNF-α水平及血清FT_3、FT_4、TSH、TPOAb、TGAb、TRAb水平。结果观察组CD3~+CD56~+NKT占淋巴细胞总数比率[(1.37±0.43)%]低于对照组[(2.47±0.39)%](P<0.05);观察组血清FT_3[(23.76±5.51)pmol/L]、FT_4[(88.29±31.35)pmol/L]、TSH[(1.68±1.01)mu/L]、TPOAb[(293.58±141.32)u/mL]、TGAb[(380.58±215.31)u/mL]、TRAb抗体[(10.75±8.23)u/mL]水平均高于对照组[FT_3(4.79±0.59)pmol/L、FT_4(17.84±3.15)pmol/L、TSH(0.08±0.01)u/L、TPOAb(20.06±4.85)u/mL、TGAb(31.48±22.68)u/mL、TRAb抗体(1.21±0.23)u/mL](P<0.05);观察组血清IL-6[(2.51±0.31)μg/L]、IL-10[(43.79±21.54)ng/L]、IL-12[(1 306.14±514.39)ng/L]、TNF-α[(4.38±0.66)ng/L]水平均高于对照组[(1.01±0.20)μg/L、(27.68±5.41)ng/L、(584.34±214.57)ng/L、(2.41±0.81)ng/L](P<0.05);观察组IL-2表达水平[(1.26±0.43)ng/L]低于对照组[(4.81±0.71)ng/L](P<0.05)。结论 Graves病患者存在免疫功能紊乱情况及免疫调节细胞失衡,通过CD3~+CD56~+NKT减少及其分泌的细胞因子调节Th1/Th2分化,参与Graves病的发病过程。
Objective To investigate the effects of natural killer T cell (NKT) and its secretion of interleukin (IL) -2, IL-6, IL-10, IL-12 and tumor necrosis factor (TNF-α) and other cytokines and free triiodothyronine (FT_3), free thyroxine (FT_4), thyroid stimulating hormone (thyroid stimulating hormone, TSH, thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TGAb) and thyrotrophin receptor antibody (TRAb) in patients with Graves disease. Methods Thirty patients with Graves disease were selected as the observation group and 30 healthy controls at the same period as the control group. The ratio of CD3 + CD56 + NKT to lymphocytes in peripheral blood and the levels of IL- 2, IL-6, IL-10, IL-12, TNF-αand serum FT_3, FT_4, TSH, TPOAb, TGAb and TRAb levels. Results The ratio of CD3 ~ + CD56 ~ + NKT to the total number of lymphocytes in the observation group was significantly lower than that in the control group [(2.47 ± 0.39)%] [(1.37 ± 0.43)%] (P <0.05) ), TPOAb [(293.58 ± 141.32) u / mL], TGAb [(380.58 ± 215.31) umol / L] / mL] and TRAb antibody [(10.75 ± 8.23) u / mL] were higher than that of the control group [FT_3 (4.79 ± 0.59) pmol / L, FT_4 (17.84 ± 3.15) pmol / TBAb (31.48 ± 22.68) u / mL and TRAb antibody (1.21 ± 0.23) u / mL] (P <0.05) IL-10 [(43.79 ± 21.54) ng / L], IL-12 [(1 306.14 ± 514.39) ng / L] and TNF-α [(4.38 ± 0.66) ng / L] (P0.01 ± 0.20) μg / L, (27.68 ± 5.41) ng / L, (584.34 ± 214.57) ng / L, (2.41 ± 0.81) ng / L] The level of IL-2 was significantly lower than that of the control group [(1.26 ± 0.43) ng / L vs (4.81 ± 0.71) ng / L, P <0.05). Conclusions There is immune dysfunction and imbalance of immunoregulatory cells in patients with Graves ’disease. The pathogenesis of Graves’ disease is involved in the regulation of Th1 / Th2 differentiation through the decrease of CD3 + CD56 + NKT and its secretion of cytokines.