本文選題：雙相障礙 + 細(xì)胞因子��； 參考：《浙江大學(xué)》2017年碩士論文

【摘要】：目的:探討雙相障礙抑郁相與外周血T細(xì)胞免疫功能的相關(guān)性,檢測患者外周血T淋巴細(xì)胞亞群和相關(guān)細(xì)胞因子IL-2、IL-4、IL-6、IL-10、TNF-α和IFN-γ的水平,以及T細(xì)胞和單核細(xì)胞表面共抑制分子TIM-3、PD-1及其配體PD-L1和PD-L2的表達(dá)。方法:采用流式細(xì)胞術(shù)測定23例雙相障礙抑郁相患者(BD)及20例健康對照(HC)外周血T淋巴細(xì)胞亞群百分含量以及T細(xì)胞和單核細(xì)胞表面共抑制分子TIM-3、PD-1及其配體PD-L1和PD-L2的表達(dá),并結(jié)合臨床參數(shù)(發(fā)病年齡、總病程、發(fā)病次數(shù)、HDRS-17評分、MADRS評分和YMRS評分)做相關(guān)分析。采用CBA法檢測 23 例 BD 患者及 20 例 HC 血清中 IL-2、IL-4、IL-6、IL-10、TNF-α 和 IFN-γ的水平。結(jié)果:雙相障礙抑郁相組外周血細(xì)胞毒性T細(xì)胞(CD3+CD8+)的表達(dá)明顯低于健康對照組(22.50±6.73 vs.29.45±6.80,P=0.002),有統(tǒng)計(jì)學(xué)差異;CD3+CD8+T細(xì)胞TIM-3+表達(dá)明顯高于健康對照組(11.45±4.15vs.7.81±2.44,P= 0.011),有統(tǒng)計(jì)學(xué)差異;單核細(xì)胞表面PD-L2的表達(dá)明顯低于健康對照組(24.90±10.84 vs.36.74±14.29,P=0.014),有統(tǒng)計(jì)學(xué)差異。相關(guān)性分析顯示:CD3+CD8+T細(xì)胞的百分含量與發(fā)病年齡呈負(fù)相關(guān)(P=0.034和ρ=0.444);CD3+CD8+T細(xì)胞TIM-3+的表達(dá)與MADRS評分呈負(fù)相關(guān)(P=0.075和ρ= 0.457)。雙相抑郁組血清IL-6表達(dá)水平明顯高于健康對照組(10.47±1.98vs.0.44±0.68,P= 0.007),有統(tǒng)計(jì)學(xué)差異;血清中IL-2、IL-4、IL-10、TNF-α和IFN-γ的表達(dá)水平均低于檢測下限,兩組間比較未發(fā)現(xiàn)有統(tǒng)計(jì)學(xué)差異。結(jié)論:1、雙相障礙抑郁相患者存在T淋巴細(xì)胞亞群的紊亂,CD3+CD8+T細(xì)胞的表達(dá)水平下降,因此檢測T淋巴細(xì)胞亞群能更客觀地反映雙相障礙抑郁相患者的T細(xì)胞免疫功能。2、雙相障礙抑郁相患者T細(xì)胞表面共抑制分子TIM-3、單核細(xì)胞表面PD-L2的表達(dá)水平出現(xiàn)了改變,提示共抑制分子可能參與了雙相障礙的發(fā)病機(jī)制,并為未來從共抑制分子水平治療雙相障礙提供理論基礎(chǔ)。3、血清IL-6的水平在BD組明顯增高,證實(shí)細(xì)胞因子的異常參與了雙相障礙抑郁相的發(fā)病機(jī)制存在關(guān)聯(lián)性。4、本研究進(jìn)一步支持了雙相障礙患者存在免疫功能的失調(diào),在未來的研究中,需要更多關(guān)注免疫抑制性分子在精神疾病中的作用。
[Abstract]:Objective: to investigate the correlation between bipolar disorder depression phase and T cell immune function in peripheral blood, and to detect the levels of TNF- 偽 and IFN- 緯 in peripheral blood T lymphocyte subsets and related cytokines IL-2, IL-4, IL-6, IL-10, TNF- 偽 and IFN- 緯 in patients with bipolar disorder. In addition, the expression of TIM-3 / PD-1 and its ligands, PD-L1 and PD-L2, on the surface of T cells and monocytes were also inhibited. Methods: flow cytometry was used to determine the percentage of T lymphocyte subsets in peripheral blood of 23 patients with bipolar disorder and 20 healthy controls, and the expression of TIM-3mPD-1 and its ligand PD-L1 and PD-L2 on the surface of T cells and monocytes. Correlation analysis was made with clinical parameters (age of onset, total course of disease, frequency of onset, HDRS-17 score, MADRS score and YMRS score). The levels of IL-2TNF- 偽 and IFN- 緯 in serum of 23 patients with BD and 20 patients with HC were detected by CBA method. Results: the expression of CD3 CD8 in peripheral blood cytotoxic T cells in bipolar disorder depression group was significantly lower than that in healthy control group (22.50 鹵6.73 vs.29.45 鹵6.80 vs.29.45 鹵6.80 P0. 002), and the expression of CD3 CD8 T cell TIM-3 was significantly higher than that in healthy control group (11.45 鹵4.15vs.7.81 鹵2.44 P = 0.011). The expression of PD-L2 on monocyte surface was significantly lower than that in healthy control group (24.90 鹵10.84 vs.36.74 鹵14.29 vs.36.74 鹵14.29 vs.36.74 鹵0.014 4). Correlation analysis showed that there was a negative correlation between the percentage of CD3 CD8 T cells and the age of onset. The expression of TIM-3 on CD3 CD8 T cells was negatively correlated with the MADRS score (P 0. 075 and 蟻 = 0. 457). The level of serum IL-6 expression in bipolar depression group was significantly higher than that in healthy control group (10.47 鹵0.68 鹵0.68 P = 0.007, P = 0.007, P = 0.007), and the levels of IL-2-, IL-4, IL-10, TNF- 偽 and IFN- 緯 in serum were lower than those in control group, and there was no significant difference between the two groups. Conclusion the expression level of CD3 CD8 T cells in the patients with bipolar disorder and depression is decreased in the presence of T lymphocyte subsets. Therefore, the detection of T lymphocyte subsets can more objectively reflect the T cell immune function of the patients with bipolar disorder and depression, the expression of TIM-3 on the surface of T cells and the expression of PD-L2 on the surface of monocytes in patients with bipolar depression. These results suggest that the co-suppressor molecules may be involved in the pathogenesis of bipolar disorder, and provide a theoretical basis for the treatment of bipolar disorders at the molecular level of co-suppression. The serum IL-6 level in BD group was significantly higher than that in BD group. It is confirmed that the abnormal cytokines are involved in the pathogenesis of bipolar disorder depression phase. 4. This study further supports the existence of disorder of immune function in patients with bipolar disorder. More attention needs to be paid to the role of immunosuppressive molecules in mental disorders.
【學(xué)位授予單位】：浙江大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R749.4

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1 鄭亞麗;雙相障礙抑郁相患者T細(xì)胞免疫功能的研究[D];浙江大學(xué);2017年

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本文編號：1795781