【摘要】：研究背景系統(tǒng)性紅斑狼瘡(Systemic lupus erythematosus,SLE),是一種好發(fā)于女性的慢性自身免疫性疾病,其臨床表現(xiàn)較為復(fù)雜,病程遷延反復(fù),常常累及多個系統(tǒng)和器官。近年來,國內(nèi)外大量研究致力于探索SLE的病因和發(fā)病機制,但其確切的機制尚未完全明了。目前一般認(rèn)為其發(fā)病涉及遺傳因素、環(huán)境因素、內(nèi)分泌狀況等多種因素,這些因素相互影響、相互作用,構(gòu)成一個復(fù)雜的病因網(wǎng),引起異常免疫反應(yīng),如炎癥因子釋放、自身抗體產(chǎn)生。SLE最初被認(rèn)為是B細(xì)胞介導(dǎo)的自身免疫性疾病。隨著研究的深入,T細(xì)胞被發(fā)現(xiàn)在SLE的發(fā)生、發(fā)展過程中也起著至關(guān)重要的作用。1999年科學(xué)家首次在果蠅體內(nèi)發(fā)現(xiàn)一種高度保守的E3泛素化連接酶蛋白,命名為Pellino(簡稱Peli)蛋白。該種泛素化連接酶蛋白家族一共有Peli-1、Peli-2、Peli-3三種亞型,其最值得一提的功能特征是在先天性免疫中承擔(dān)多元性角色。最新研究發(fā)現(xiàn)Peli-1在參與TLR/IL-1R介導(dǎo)的一系列細(xì)胞信號傳導(dǎo)起著一定的調(diào)節(jié)作用。Peli-1還參與介導(dǎo)TRIF依賴的NF-κB活化。此外,Chang等發(fā)現(xiàn)Peli-1是維持T細(xì)胞耐受的一個關(guān)鍵調(diào)節(jié)因子,其功能異�？赡軐�(dǎo)致T細(xì)胞激活,從而可能在SLE等自身免疫性疾病的發(fā)病中起重要作用�；谝陨蟽�(nèi)容,本課題首次探討Peli-1基因多態(tài)性與SLE的疾病易感性之間的關(guān)聯(lián);同時檢測Peli-1 mRNA表達水平及其與SLE易感性和SLE不同表型之間的相關(guān)性,從基因轉(zhuǎn)錄、表達水平分別探討Peli-1基因與SLE發(fā)病之間的關(guān)系。第一部分peli-1基因單核苷酸多態(tài)性與系統(tǒng)性紅斑狼瘡的相關(guān)性研究目的比較sle患者于正常對照peli-1rs329498、rs10496105等位基因和基因頻率的差異,探討其與sle遺傳易感性的關(guān)聯(lián)。并結(jié)合臨床資料,分析peli-1rs329498、rs10496105與其主要臨床特征及其實驗室指標(biāo)之間的關(guān)系。方法采用病例對照的研究方法,選取738名sle患者和827名健康對照。采用fluidigm192.24基因分型技術(shù)檢測peli-1基因中rs329498、rs10496105兩個snp位點,對其基因型、等位基因頻率等進行分析,并結(jié)合臨床資料進一步分析基因頻率分布于臨床表現(xiàn)之間的關(guān)系。結(jié)果(1)peli-1基因rs329498位點多態(tài)性與sle的關(guān)聯(lián)性研究sle患者組aa、ac、cc的基因型頻率分別為40.8%、44.6%、14.6%,對照組分別為36.5%、45.5%、18.0%,兩組差異無統(tǒng)計學(xué)意義(χ2=4.63,p=0.099)。等位基因比較顯示兩組差異有統(tǒng)計學(xué)意義(χ2=4.80,p=0.028),相對大等位基因a,小等位基因c會降低sle發(fā)病的風(fēng)險(or=0.851,95%ci:0.737-0.983)。但遺傳顯性、隱性模型均未見統(tǒng)計學(xué)關(guān)聯(lián)(均有p0.05)。與非ln腎炎組患者相比,ln患者a等位基因頻率較高,且差異有統(tǒng)計學(xué)意義(χ2=8.18,p=0.017)。小等位基因c相比于a等位基因,其ln發(fā)病風(fēng)險or值為0.681(95%ci:0.528-0.880)。兩組顯性模型基因型頻率(cc+acversusaa)分布差異有統(tǒng)計學(xué)意義(or=0.632,95%ci:0.451-0.884,p=0.007)。臨床特征關(guān)聯(lián)性分析顯示peli-1基因rs329498位點可能與顴部紅斑有關(guān),其基因型頻率分布有統(tǒng)計學(xué)差異(χ2=6.63,p=0.036)。(2)peli-1基因rs10496105位點多態(tài)性與sle的關(guān)聯(lián)性研究位點rs10496105基因型頻率gg、ag、aa在病例組分別為70.0%、26.2%和3.8%,對照組中分別為69.4%,27.2%和3.4%。病例組與對照組基因型頻率分布無統(tǒng)計學(xué)差異(χ2=0.37,p=0.832)。遺傳模型分析結(jié)果表明,無論是顯性模型還是隱性模型病例組和對照組分布均未發(fā)現(xiàn)統(tǒng)計學(xué)差異(均有p0.05)。此外,ln組與非LN組間基因型分布差異無統(tǒng)計學(xué)意義(χ2=3.11,P=0.201)。臨床資料分析結(jié)果顯示rs10496105位點與顴部紅斑、盤狀紅斑、光敏感、口腔潰瘍、關(guān)節(jié)炎等主要臨床特征也無統(tǒng)計學(xué)關(guān)聯(lián)(均有P0.05)。結(jié)論中國漢族人群中Peli-1 rs329498基因多態(tài)性與SLE遺傳易感性有一定關(guān)聯(lián),此外,rs329498位點也與狼瘡腎炎及顴部紅斑有關(guān)。而未發(fā)現(xiàn)rs10496105基因多態(tài)性位點與SLE之間的統(tǒng)計學(xué)關(guān)聯(lián)。第二部分Peli-1 m RNA水平與系統(tǒng)性紅斑狼瘡的相關(guān)性研究目的分別比較SLE患者組和正常對照組、SLE患者中狼瘡腎炎組與非狼腎炎組以及活動組與非活動組外周血單個核細(xì)胞(Peripheral blood mononuclear cells,PBMCs)中Peil-1基因m RNA表達水平,并探討其表達水平與臨床特征、實驗室指標(biāo)以及疾病活動度之間的關(guān)系。方法共收集31例SLE患者和30例健康對照。采用Trizol法提取PBMCs中的RNA。實時定量聚合酶鏈反應(yīng)(Real time quantitative polymerase chain reaction,RT-PCR)檢測PBMCs中的Peli-1基因m RNA表達水平,利用Mann-Whitney秩和檢驗比較各組之間m RNA水平是否存在差異。采用Spearman相關(guān)分析Peli-1基因m RNA表達水平與系統(tǒng)性紅斑狼瘡疾病活動指數(shù)(Systemic lupus erythematosus disease activity index,SLEDAI)關(guān)系。所有數(shù)據(jù)均采用SPSS 17.0進行統(tǒng)計分析。結(jié)果(1)PBMCs中Peli-1 m RNA表達水平比較:31例SLE患者與30例對照組PBMCs中的Peli-1 m RNA水平無統(tǒng)計學(xué)差異(Z=-0.404,P=0.686)。將SLE患者分為腎炎組(11例)和非腎炎組(20例)比較,結(jié)果顯示兩組PBMCs中的Peli-1m RNA水平無統(tǒng)計學(xué)差異(Z=-0.619,P=0.536)。此外,活動組(19例)和非活動組(12例)組間的PBMCs中的Peli-1 m RNA水平無統(tǒng)計學(xué)差異(Z=-0.973,P=0.330)。(2)SLE患者PBMCs中Peli-1 m RNA水平與其臨床特征關(guān)聯(lián)性分析:Mann-Whitney秩和檢驗結(jié)果顯示,各組之間Peli-1 m RNA水平差異均無統(tǒng)計學(xué)意義(均有P0.05)。(3)SLE患者PBMCs中Peli-1 m RNA水平與實驗室指標(biāo)關(guān)聯(lián)性分析:各個實驗室指標(biāo)陽性組與陰性組間Peli-1 m RNA水平差異均無統(tǒng)計學(xué)意義(均有P0.05)。(4)SLE患者PBMCs中Peli-1 m RNA表達水平與SLEDAI相關(guān)性分析:Spearman等級相關(guān)分析結(jié)果顯示,SLE患者PBMCs中Peli-1 m RNA水平與SLEDAI評分之間無明顯相關(guān)性(rs=0.148,P=0.428)。結(jié)論本研究發(fā)現(xiàn)SLE患者與健康對照組、患者活動組與非活動組、LN與非LN組之間Peli-1基因m RNA表達水平無統(tǒng)計學(xué)差異。此外,通過分析比較各主要臨床表現(xiàn)及實驗室主要特征,結(jié)果也均未發(fā)現(xiàn)統(tǒng)計學(xué)差異。SLEDAI評分與Peli-1基因m RNA表達水平也無明顯相關(guān)性。
[Abstract]:Research background systemic lupus erythematosus (Systemic lupus erythematosus, SLE) is a kind of chronic autoimmune disease in women. Its clinical manifestation is more complex, the course of disease is prolonged, and many systems and organs are often involved. In recent years, a lot of studies have been made to explore the etiology and pathogenesis of SLE, but the exact mechanism of it has been studied. It is not yet fully understood. It is generally considered to be associated with a variety of factors such as genetic, environmental and endocrine factors that interact and interact to form a complex network of etiological factors that cause abnormal immune responses, such as the release of inflammatory factors, and the production of.SLE by autoantibodies is initially considered to be an autoimmune disease mediated by B cells. Disease. With the development of research, T cells have been found to occur in SLE and also play a vital role in the development of.1999. A highly conserved E3 ubiquitin ligase protein, named Pellino (abbreviated Peli) protein, was found in the fruit fly for the first time. The ubiquitin ligase protein family consists of Peli-1, Peli-2, Peli-3 three. The most notable functional feature of the subtype is the multiple role in innate immunity. The latest research has found that Peli-1 plays a regulatory role in a series of cellular signaling mediated by TLR/IL-1R,.Peli-1 also participates in the activation of NF- kappa B, which is mediated by TRIF dependence. In addition, Chang has found that Peli-1 is one of the maintenance of T cell tolerance. A key regulatory factor, whose functional abnormalities may lead to T cell activation, may play an important role in the pathogenesis of autoimmune diseases such as SLE. Based on the above, this subject is the first to explore the association between the Peli-1 gene polymorphism and the susceptibility to the disease of SLE, and also to detect the expression level of Peli-1 mRNA and the susceptibility to SLE and SLE. The correlation between the same phenotype, the relationship between the Peli-1 gene and the incidence of SLE from the gene transcription and expression level. The correlation between the single nucleotide polymorphisms of the peli-1 gene and systemic lupus erythematosus (SLE) in part 1 compares the difference between the SLE patients and the difference of the peli-1rs329498, rs10496105 allele and gene frequency in the normal control. The association with the genetic susceptibility of SLE. Combined with clinical data, the relationship between peli-1rs329498, rs10496105 and its main clinical features and its laboratory indicators was analyzed. Methods a case control study was used to select 738 SLE patients and 827 healthy controls. The fluidigm192.24 gene typing technique was used to detect rs329498 in the peli-1 gene. Rs10496105 two SNP loci, analysis of its genotype, allele frequency and so on. Combined with clinical data, the relationship between gene frequency distribution and clinical manifestations was further analyzed. Results (1) the association between the polymorphism of peli-1 gene rs329498 locus and SLE, the genotype frequencies of AA, AC and CC in SLE patients were 40.8%, 44.6%, and 14.6%, respectively. There was no statistically significant difference between the groups of 36.5%, 45.5%, 18% and two groups (x 2=4.63, p=0.099). The allele comparison showed that the two groups were statistically significant (x 2=4.80, p=0.028), relatively large allele A, and small allele C would reduce the risk of SLE incidence (or= 0.851,95%ci:0.737-0.983). However, there was no statistical correlation between the genetic dominance and the recessive model. Compared with the non ln nephritis group, the A allele frequency of LN patients was higher, and the difference was statistically significant (x 2=8.18, p=0.017). The or value of LN incidence risk was 0.681 (95%ci:0.528-0.880) compared with the A allele, and the difference in the genotype frequency (cc+acversusaa) distribution of the two groups was statistically significant. .632,95%ci:0.451-0.884, p=0.007). The correlation analysis of clinical features showed that the rs329498 locus of the peli-1 gene might be related to the zygomatic erythema, and the frequency distribution of the genotypes was statistically different (x 2=6.63, p=0.036). (2) the association of the peli-1 gene rs10496105 loci with SLE was associated with the rs10496105 genotype frequency GG, Ag, in the case component. No 70%, 26.2% and 3.8%, 69.4% in the control group, 27.2% and 3.4%., and no statistical difference between the control group and the control group (x 2=0.37, p=0.832). The genetic model analysis showed that no statistical difference was found between the dominant and the recessive model cases and the control groups (P0.05). In addition, the LN group and the LN group There was no statistically significant difference in genotype distribution between non LN groups (x 2=3.11, P=0.201). The results of clinical data analysis showed that there was no statistically significant association between the rs10496105 locus and the main clinical features of the zygomatic erythema, discoid erythema, light sensitivity, oral ulcer, and arthritis (P0.05). The polymorphism of the Peli-1 rs329498 gene and SLE remains in the Chinese Han population. In addition, the rs329498 locus was also associated with lupus nephritis and zygomatic erythema. No statistical association was found between the rs10496105 gene polymorphisms and SLE. Second the correlation between the Peli-1 m RNA level and systemic lupus erythematosus was compared with those in the SLE group and the normal control group, and the wolves in SLE patients. The expression level of Peil-1 gene m RNA in Peripheral blood mononuclear cells (PBMCs) in the group of ulcer nephritis and non wolf nephritis and in the active group and non active group (mononuclear cells, PBMCs), and the relationship between the expression level and clinical characteristics, the laboratory index and the degree of disease activity. Methods a total of 31 cases of SLE patients and 30 healthy pairs were collected. Trizol method was used to extract the RNA. real-time quantitative polymerase chain reaction (Real time quantitative polymerase chain reaction, RT-PCR) to detect the Peli-1 gene expression level in PBMCs, using the rank sum test to compare the differences between each group. The relationship between the level and the Systemic lupus erythematosus disease activity index, SLEDAI. All data were statistically analyzed with SPSS 17. Results (1) the level of Peli-1 m RNA in PBMCs was compared: there was no statistical difference between the 31 cases and the 30 controls. 404, P=0.686). Compared the SLE patients into the nephritis group (11 cases) and the non nephritis group (20 cases), the results showed that there was no statistical difference between the two groups of PBMCs (Z=-0.619, P=0.536). Moreover, the Peli-1 m RNA level between the active group (19 cases) and the non active group (12 cases) had no statistical difference (Z=-0.973, 2). The correlation analysis of Peli-1 m RNA level and its clinical characteristics: the Mann-Whitney rank sum test results showed that there was no statistical significance (P0.05) between the Peli-1 m RNA levels between each group. (3) the correlation between Peli-1 m level and laboratory index in PBMCs of SLE patients: the difference between the positive group and the negative group was poor. There was no statistical significance (all P0.05). (4) the level of Peli-1 m RNA expression in PBMCs of SLE patients and SLEDAI correlation analysis: Spearman grade correlation analysis showed that there was no significant correlation between Peli-1 m in SLE patients' PBMCs and the health control group. There was no statistical difference between the Peli-1 gene m RNA expression level between the LN and the non LN groups in the dynamic group and the non active group. In addition, there was no statistical difference between the major clinical manifestations and the major laboratory features, and there was no statistically significant difference between the.SLEDAI score and the RNA expression level of the Peli-1 gene m.
【學(xué)位授予單位】：安徽醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：R593.241

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