發(fā)布時(shí)間：2018-05-29 01:45

  本文選題：Ig + A腎病��； 參考：《鄭州大學(xué)》2015年博士論文

【摘要】：研究背景： Ig A腎病(Ig A nephropathy,Ig AN)是我國(guó)乃至全球最常見(jiàn)的原發(fā)性腎小球腎炎,其特征是免疫熒光下見(jiàn)到以Ig A為主的免疫復(fù)合物在腎小球系膜區(qū)和/或腎小球毛細(xì)血管襻沉積。據(jù)2014年最新資料顯示,全球Ig AN的發(fā)病率為2.5人/10萬(wàn)人/每年,約20%-50%的患者20年可進(jìn)展為終末期腎臟病。但是,Ig AN的發(fā)病機(jī)制仍然不十分清楚。因Ig AN患者常在上呼吸道或腸道等粘膜感染后發(fā)生肉眼血尿和/或蛋白尿,提示粘膜免疫與Ig AN的發(fā)病機(jī)制密切相關(guān)。分泌型Ig A(secretory Ig A,SIg A)是參與粘膜免疫最重要的抗體,近年來(lái)的研究發(fā)現(xiàn),SIg A在Ig AN的發(fā)病中可能也起著一定的致病作用。Ig AN的病理類型及臨床表現(xiàn)具有多樣性,是否因?yàn)橛蠸Ig A的參與?SIg A可以沉積在Ig AN患者的系膜區(qū),那么它對(duì)系膜細(xì)胞具有損傷作用嗎?SIg A發(fā)揮這些致病損傷作用的機(jī)制是什么呢?迄今為止,還未見(jiàn)相關(guān)報(bào)道。Micro RNAs(mi RNAs)是真核生物中一類具有內(nèi)源性調(diào)控功能的非編碼RNA,它通過(guò)與靶基因信使RNA(messenger RNA,m RNA)的3’端非編碼區(qū)(untranslated region,UTR)結(jié)合,發(fā)揮抑制翻譯的作用。研究提示,mi RNAs在腎臟病中也起了重要的作用。那么SIg A是否通過(guò)作用mi RNAs來(lái)發(fā)揮在Ig AN中的致病性呢?第一部分Ig A腎病患者分泌型Ig A在腎組織的沉積以及同臨床病理之間的關(guān)系目的： 檢測(cè)Ig AN患者腎組織中SIg A沉積的比例;分析SIg A與臨床及腎臟病理之間的關(guān)系。方法：選取263名原發(fā)性Ig AN患者,應(yīng)用激光共聚焦顯微鏡觀察腎組織SIg A的沉積,并比較有SIg A沉積和無(wú)沉積患者的臨床及腎臟病理各項(xiàng)指標(biāo)的不同。結(jié)果： 1.263名Ig AN患者中87名可見(jiàn)到系膜區(qū)SIg A的沉積,約占29.28%;2.同系膜區(qū)無(wú)SIg A沉積的病人相比較,有SIg A沉積的病人具有明顯的感染史(P=0.016)及血尿(P=0.024)發(fā)生率,臨床指標(biāo)上具有明顯低水平的血清胱抑素C(P=0.027)和β2微球蛋白(P=0.018),病理特征上具有更微的腎臟小管間質(zhì)損傷(P=0.030)和更低的T評(píng)分(牛津分型,P=0.026)。結(jié)論： 粘膜免疫同Ig AN密切相關(guān),SIg A參與了Ig AN的發(fā)病,它在腎組織的沉積與某些的臨床腎臟病理指標(biāo)相聯(lián)系。第二部分分泌型Ig A在Ig AN患者腎組織激活的補(bǔ)體通路研究目的： 檢測(cè)Ig AN患者腎組織中SIg A激活的補(bǔ)體通路來(lái)研究SIg A的腎損傷作用,以及比較腎組織經(jīng)不同補(bǔ)體途徑激活的Ig AN患者之間的臨床病理特征。方法： 選取87名原發(fā)性IgAN患者,應(yīng)用激光共聚焦顯微鏡觀察腎組織SIgA以及各補(bǔ)體通路相關(guān)蛋白的沉積,探討SIg A與各補(bǔ)體通路激活的關(guān)系,并比較不同補(bǔ)體激活通路的患者臨床及腎病理特點(diǎn)之間的差別。結(jié)果： 1.87名IgAN患者中有22名可見(jiàn)到系膜區(qū)SIgA沉積,其中經(jīng)旁路途徑激活的占77.27%,在65名無(wú)SIg A沉積的患者中經(jīng)凝集素途徑激活的占72.30%,兩組比較無(wú)明顯差別(P=0.648);2.同腎組織經(jīng)凝集素途徑激活的患者相比較,經(jīng)旁路途徑激活的64人(73.6%)在臨床指標(biāo)方面具有更低的腎小球?yàn)V過(guò)率(P=0.043),在腎病理方面腎小球硬化比例(P=0.035)、小管間質(zhì)損傷程度(P=0.030)、C3的免疫熒光強(qiáng)度(P=0.012)以及牛津評(píng)分的S(P=0.006)和T評(píng)分(P=0.039)均損傷更嚴(yán)重。結(jié)論： 在Ig AN中SIg A具有致病性,可能通過(guò)激活旁路途徑和凝集素途徑造成腎損傷;經(jīng)旁路途徑激活的Ig AN患者部分臨床和腎病理特征比經(jīng)凝集素途徑激活的患者嚴(yán)重。第三部分分泌型Ig A對(duì)系膜細(xì)胞的生物學(xué)效應(yīng)研究目的： 研究SIgA對(duì)人系膜細(xì)胞的生物學(xué)效應(yīng),探討SIgA在IgAN中的致病作用。方法： 運(yùn)用親和層析柱提純Ig AN患者及正常人唾液中的SIg A,應(yīng)用親和層析柱和分子篩提純Ig AN患者及正常人血中的多聚Ig A(polymeric Ig A,p Ig A);將提純的SIg A及p Ig A分別刺激人系膜細(xì)胞,檢測(cè)細(xì)胞的增殖及各種促炎促纖維化因子(IL-6、IL-8、MCP-1、TGF-β1和纖維粘連蛋白)在細(xì)胞中m RNA及蛋白水平的表達(dá)情況,并相互比較。結(jié)果： 1.SIg A和p Ig A均能使人系膜細(xì)胞明顯增殖(P0.05),表達(dá)IL-6、IL-8、MCP-1、TGF-β1和纖維粘連蛋白明顯增多(m RNA和蛋白水平,P0.05),并且患者來(lái)源的SIg A和p Ig A對(duì)細(xì)胞的上述生物學(xué)效應(yīng)均明顯強(qiáng)于正常人來(lái)源的刺激作用(P0.05);2.經(jīng)Ig AN患者唾液純化的SIg A對(duì)系膜細(xì)胞的增殖作用及刺激其分泌IL-6、IL-8和纖維粘連蛋白的作用要明顯弱于經(jīng)Ig AN患者血清純化的p Ig A作用(P0.05)。結(jié)論：在Ig AN中SIg A有致病作用,SIg A具有刺激系膜細(xì)胞增殖和釋放促炎促纖維化細(xì)胞因子的生物學(xué)效應(yīng),并且SIg A與p Ig A對(duì)系膜細(xì)胞的生物學(xué)效應(yīng)是不完全相同的。第四部分與分泌型Ig A致病性有關(guān)的micro RNAs篩選及驗(yàn)證目的： 篩選與SIg A致病性有關(guān)的mi RNAs,研究SIg A在Ig AN中產(chǎn)生致病性的分子機(jī)制。方法： 運(yùn)用Agilent human mi RNAs芯片,檢測(cè)經(jīng)Ig AN患者及正常人SIg A刺激的系膜細(xì)胞中的mi RNAs,并分析篩選其中差異性表達(dá)的mi RNAs,應(yīng)用實(shí)時(shí)熒光定量PCR分別進(jìn)行驗(yàn)證。結(jié)果： 1.通過(guò)mi RNAs芯片篩選了17個(gè)經(jīng)Ig AN患者及正常人的SIg A刺激后細(xì)胞內(nèi)差異表達(dá)的mi RNAs,其中上調(diào)5個(gè)、下調(diào)12個(gè);2.經(jīng)實(shí)時(shí)熒光定量PCR驗(yàn)證芯片篩選結(jié)果中的mi RNAs,趨勢(shì)均一致,其中16個(gè)表達(dá)差異顯著(P0.05),1個(gè)差異性不顯著(P0.05)。結(jié)論： SIgA在IgAN發(fā)揮致病性的機(jī)制中,mi RNAs參與其中。第五部分mi R-16-2-3p和mi R-100-3p調(diào)控IL-6和IL-8的分子機(jī)制目的： 預(yù)測(cè)和驗(yàn)證了miR-16-2-3p和mi R-100-3p的靶基因,進(jìn)一步探討SIgA在Ig AN中產(chǎn)生致病性的分子機(jī)制。方法：通過(guò)生物信息學(xué)方法對(duì)mi RNAs芯片篩選結(jié)果中的mi R-16-2-3p和mi R-100-3p進(jìn)行靶基因預(yù)測(cè),建立融合靶基因3‘UTR的熒光素酶報(bào)告基因載體,通過(guò)雙報(bào)告熒光素酶基因檢測(cè)方法確定mi R-16-2-3p和mi R-100-3p的靶基因;應(yīng)用實(shí)時(shí)熒光定量PCR和Western blot研究mi R-16-2-3p和mi R-100-3p對(duì)其靶基因的內(nèi)源性調(diào)控作用。結(jié)果： 1.成功構(gòu)建了能夠過(guò)表達(dá)mi R-16-2-3p和mi R-100-3p的報(bào)告基因載體;2.熒光素酶雙報(bào)告基因檢測(cè)顯示,mi R-16-2-3p和mi R-100-3p的復(fù)制物可以分別與報(bào)告基因載體的IL-6和IL-8 3’UTR野生序列結(jié)合,使載體的熒光素酶活性降低,而IL-6和IL-8 3’UTR突變序列不能產(chǎn)生這樣的作用(P0.05);3.Mi R-16-2-3p過(guò)表達(dá)可以抑制SIg A刺激系膜細(xì)胞中分泌IL-6蛋白過(guò)多的情況,但不影響IL-6 m RNA的水平(P0.05),同樣mi R-100-3p過(guò)表達(dá)可以抑制其分泌IL-8蛋白過(guò)多的情況,但不能影響IL-8 m RNA的水平(P0.05)。結(jié)論： Mi R-16-2-3p的靶基因是IL-6,mi R-100-3p的靶基因是IL-8;SIg A通過(guò)作用mi R-16-2-3p和mi R-100-3p來(lái)分別調(diào)控系膜細(xì)胞產(chǎn)生炎癥因子IL-6和IL-8,是SIg A在Ig AN中產(chǎn)生致病性的分子機(jī)制之一。全文結(jié)論 SIg A參與了Ig AN的發(fā)病,它在腎組織的沉積同一定的臨床腎臟病理指標(biāo)相聯(lián)系;SIg A在Ig AN中具有致病作用,表現(xiàn)在有可能激活旁路途徑和凝集素途徑造成腎損傷,刺激系膜細(xì)胞增殖并釋放促炎促纖維化細(xì)胞因子;SIg A通過(guò)作用mi R-16-2-3p和mi R-100-3p來(lái)分別調(diào)控系膜細(xì)胞產(chǎn)生炎癥因子IL-6和IL-8,可能是SIg A在Ig AN中發(fā)揮致病作用的機(jī)制之一。
[Abstract]:Background: Ig A nephropathy (Ig A nephropathy, Ig AN) is the most common primary glomerulonephritis in China and in the world. It is characterized by the deposition of Ig A based immune complexes in the glomerular mesangial region and / or glomerular capillary loops under immunofluorescence. According to the latest data in 2014, the incidence of Ig AN in the global Ig is 2.5 people. People / each year, about 20%-50% patients can progress to end-stage renal disease in 20 years. However, the pathogenesis of Ig AN is still not very clear. Because Ig AN patients often occur naked hematuria and / or proteinuria after infection of the upper respiratory tract or intestinal mucosa, suggesting that mucosal immunity is closely related to the pathogenesis of Ig AN. Secretory Ig A (secretory Ig A) It is the most important antibody involved in mucosal immunization. Recent studies have found that SIg A may also play a certain pathogenicity in the pathogenesis of Ig AN in the pathological type and clinical manifestations of.Ig AN. Is there the participation of SIg A? SIg A can be deposited in the mesangial region of Ig AN patients, and is it damaging to mesangial cells? What is the mechanism of Ig A playing these pathogenetic effects? So far, no related reports have been reported that.Micro RNAs (MI RNAs) is a non coded RNA with endogenous regulatory functions in eukaryotes, which combines with the 3 'end non coding region of the target gene messenger RNA (messenger RNA, m RNA) and exerts inhibition. The study suggests that MI RNAs plays an important role in renal disease. Then, does SIg A play the pathogenicity in Ig AN by acting mi RNAs? Analysis of the relationship between SIg A and clinical and renal pathology. Methods: 263 patients with primary Ig AN were selected and the deposition of SIg A in renal tissue was observed by laser confocal microscopy, and the clinical and renal pathological indexes of SIg A and non deposition patients were compared. Fruit: 87 of the 1.263 Ig AN patients could see the mesangial region. The deposition of SIg A accounted for about 29.28%; 2. compared with patients without SIg A deposition in the homologous membrane region, the patients with SIg A deposition had obvious infection history (P=0.016) and hematuria (P=0.024), and the clinical indicators had obvious low levels of serum cystatin C (P=0.027) and beta 2 microglobulin (P=0.018), and the pathological features had a slightly smaller tubulointerstitium. Damage (P=0.030) and lower T score (Oxford classification, P=0.026). Conclusion: mucosal immunity is closely related to Ig AN, SIg A participates in the pathogenesis of Ig AN, and its deposition in the renal tissue is associated with some clinical renal pathological indexes. Second part secretory Ig A in the renal tissue activated complement pathway of the Ig patients: detection The role of SIg A activated complement pathway in renal tissue to study the renal damage of SIg A and to compare the clinicopathological features of Ig AN patients activated by different complement pathways in renal tissue. Methods: 87 primary IgAN patients were selected to observe the deposition of SIgA in renal tissue and the proteins related to complement pathway by laser confocal microscopy. The relationship between SIg A and the activation of complement pathway was investigated and the difference between the clinical and renal pathological features of the patients with different complement activation pathways was compared. Results: 22 of the 1.87 IgAN patients could see the SIgA deposition in the mesangial region, among which 77.27% were activated by the bypass pathway, and 7 of the 65 patients without SIg A were activated by the agglutinin pathway. 2.30%, there was no significant difference in the two groups (P=0.648); 2. the 64 (73.6%) activated by the bypass pathway (73.6%) had lower glomerular filtration rate (P=0.043), renal pathological glomerular sclerosis ratio (P=0.035), tubulointerstitial damage (P=0.030), and C3 immunofluorescence Light intensity (P=0.012) and the S (P=0.006) and T score (P=0.039) of the Oxford score were more severe. Conclusion: SIg A in Ig AN is pathogenicity and may cause renal injury by activating the bypass pathway and lectin pathway; some of the clinical and renal pathological features of Ig AN patients activated by the bypass pathway are more severe than those activated by the lectin pathway. The biological effects of third partial secretory Ig A on mesangial cells: To study the biological effects of SIgA on human mesangial cells and to explore the pathogenicity of SIgA in IgAN. Methods: purification of SIg A in Ig AN patients and normal human saliva by affinity chromatography column, and the purification of Ig AN patients and normal by affinity chromatography column and molecular sieve. Ig A (polymeric Ig A, P Ig A) in human blood, and the purified SIg A and P Ig, respectively, to stimulate human mesangial cells and to detect the proliferation of cells and the expression of various proinflammatory fibrotic factors in cells. The proliferation of human mesangial cells (P0.05), IL-6, IL-8, MCP-1, TGF- beta 1 and fibronectin were significantly increased (m RNA and protein level, P0.05), and the biological effects of SIg A and P Ig from the patients were significantly stronger than those of normal human sources. 2. The proliferation and stimulation of the secretion of IL-6, IL-8 and fibronectin should be significantly weaker than the P Ig A action (P0.05) purified by Ig AN patients. Conclusion: SIg A in Ig AN has the pathogenicity, which has the biological effect of stimulating mesangial cell proliferation and releasing proinflammatory cytokines. The biological effects of the cells are not exactly the same. Fourth the screening and verification of micro RNAs related to the pathogenicity of the secretory Ig A is to screen the MI RNAs related to the pathogenicity of SIg A and to study the molecular mechanism of the pathogenesis of SIg A in Ig AN. The MI RNAs in the mesangial cells stimulated by A was analyzed and the differential expression of MI RNAs was screened, and the real-time fluorescent quantitative PCR was used to verify the results. Results: 1. through mi RNAs chip, 17 cells were screened by Mi RNAs chip and the differential expression in the cells after SIg A stimulation, up regulation 5, down 12; 2. by real time fluorescence determination. The trend of MI RNAs in the screening results of PCR was the same, and the 16 differences were significant (P0.05) and 1 differences were not significant (P0.05). Conclusion: SIgA is involved in the pathogenesis of IgAN, MI RNAs participates in it. Fifth part mi R-16-2-3p and Mi regulates and regulates the molecular mechanisms. The target genes of 6-2-3p and MI R-100-3p further explore the molecular mechanism of the pathogenicity of SIgA in Ig AN. Method: target gene prediction of MI R-16-2-3p and MI R-100-3p in the screening results of MI RNAs chips by bioinformatics method, and to establish a fusion target gene 3 'fluorescein reporter gene carrier, through double reporting fluorescein. The target genes of MI R-16-2-3p and MI R-100-3p were determined by enzyme gene detection. The endogenous regulatory effects of MI R-16-2-3p and MI R-100-3p on the target genes were studied by real time fluorescent quantitative PCR and Western blot. Results: 1. the reporter gene vector was successfully constructed and the 2. luciferase double reporter gene was successfully constructed. The results showed that the replication of MI R-16-2-3p and MI R-100-3p could be combined with the IL-6 and IL-8 3 'UTR wild sequence of the reporter gene vector, and the luciferase activity of the carrier was reduced, while IL-6 and IL-8 3' UTR mutation sequence could not produce such action. L-6 protein is too much, but it does not affect the level of IL-6 m RNA (P0.05), and the overexpression of MI R-100-3p can inhibit its secretion of IL-8 protein, but it can not affect the IL-8 m RNA level. The formation of inflammatory factors IL-6 and IL-8 respectively in mesangial cells is one of the molecular mechanisms of the pathogenesis of SIg A in Ig AN. Conclusion SIg A is involved in the pathogenesis of Ig AN, and its deposition in the renal tissue is associated with a certain clinical renal pathological index; SIg A has a pathogenic role in the pathogenesis of the bypass pathway and the possibility of activating the bypass pathway and coagulation. The collection pathway causes renal injury, stimulates the proliferation of mesangial cells and releases proinflammatory cytokines, and SIg A regulates the inflammatory factors IL-6 and IL-8 by Mi R-16-2-3p and MI R-100-3p, which may be one of the mechanisms of SIg A in Ig AN.
【學(xué)位授予單位】：鄭州大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2015
【分類號(hào)】：R692.31

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1 楊光;王加啟;哈斯額爾敦;趙圣國(guó);劉開(kāi)朗;卜登攀;;牛乳中sIgA的合成機(jī)理及提高技術(shù)[A];中國(guó)奶業(yè)協(xié)會(huì)年會(huì)論文集2009（下冊(cè)）[C];2009年

2 吳舊生;;腸道菌群變化對(duì)實(shí)驗(yàn)小鼠腸黏膜sIgA表達(dá)的影響[A];中國(guó)畜牧獸醫(yī)學(xué)會(huì)動(dòng)物解剖學(xué)及組織胚胎學(xué)分會(huì)第十七次學(xué)術(shù)研討會(huì)論文集（下）[C];2012年

3 張銀旺;榮媛;;SIgA水平對(duì)白色念珠菌粘附陰道上皮細(xì)胞的影響[A];湖北省暨武漢市微生物學(xué)會(huì)分析微生物專業(yè)委員會(huì)第十屆第五次學(xué)術(shù)會(huì)議論文匯編[C];2008年

4 段小花;李嫻;康海虹;李秀芳;林青;;解表方對(duì)寒冷刺激小鼠唾液中SIgA含量和溶菌酶活性的影響[A];中華中醫(yī)藥學(xué)會(huì)中藥實(shí)驗(yàn)藥理分會(huì)第八屆學(xué)術(shù)會(huì)議論文摘要匯編[C];2009年

5 馮志新;逯曉敏;劉茂軍;吳敘蘇;甘源;邵國(guó)青;;利用SIgA-ELISA建立豬肺炎支原體感染的檢測(cè)方法[A];中國(guó)畜牧獸醫(yī)學(xué)會(huì)2009學(xué)術(shù)年會(huì)論文集（上冊(cè)）[C];2009年

6 李浩;;肺虛實(shí)證候患者上下呼吸道脫落細(xì)胞及SIgA變化的對(duì)比分析[A];第三屆第四次全國(guó)中西醫(yī)結(jié)合耳鼻咽喉科學(xué)術(shù)會(huì)論文匯編[C];2002年

7 劉明華;張慶玲;文亮;向強(qiáng);鄧朝霞;張雷;;機(jī)械通氣病人胃液SIgA含量和pH值與胃內(nèi)細(xì)菌定植的關(guān)系[A];第十一次全國(guó)急診醫(yī)學(xué)學(xué)術(shù)會(huì)議暨中華醫(yī)學(xué)會(huì)急診醫(yī)學(xué)分會(huì)成立二十周年慶典論文匯編[C];2006年

8 周華波;房慧伶;賈永起;王曉麗;吳欣欣;李紅蕾;;傳染性支氣管炎弱毒苗黏膜免疫途徑對(duì)雛雞上呼吸道及哈德氏腺SIgA細(xì)胞分布的影響[A];中國(guó)畜牧獸醫(yī)學(xué)會(huì)動(dòng)物解剖學(xué)及組織胚胎學(xué)分會(huì)第十四次學(xué)術(shù)研討會(huì)論文集[C];2006年

9 汪常偉;李凡成;;綜合療法對(duì)常年性變態(tài)反應(yīng)性鼻炎患者SIgA、IgE水平的影響[A];世界中聯(lián)耳鼻喉口腔科專業(yè)委員會(huì)第五屆學(xué)術(shù)年會(huì)、中華中醫(yī)藥學(xué)會(huì)耳鼻喉科分會(huì)第十九屆學(xué)術(shù)交流會(huì)暨貴州省中西醫(yī)結(jié)合學(xué)會(huì)耳鼻咽喉分會(huì)第二次學(xué)術(shù)交流會(huì)論文匯編[C];2013年

10 楊利林;羅頌平;朱玲;;生殖道局部sIgA的作用及研究進(jìn)展[A];全國(guó)中西醫(yī)結(jié)合生殖系統(tǒng)炎癥性疾病專題學(xué)術(shù)會(huì)議論文及摘要集[C];2013年

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1 劉建軍;IgA在粘膜抗流感免疫中起重要的作用[N];中國(guó)高新技術(shù)產(chǎn)業(yè)導(dǎo)報(bào);2001年

相關(guān)博士學(xué)位論文 前4條

1 劉冬妍;急性肝壞死時(shí)腸道SIgA變化機(jī)制的研究[D];中國(guó)醫(yī)科大學(xué);2006年

2 陳超;金欣口服液調(diào)節(jié)RSV感染模型TNF-αmRNA、SIgA表達(dá)及干預(yù)融合病變的實(shí)驗(yàn)研究[D];南京中醫(yī)藥大學(xué);2011年

3 王縛鯤;重組人抗幽門螺桿菌尿素酶B亞單位sIgA分子的構(gòu)建表達(dá)及特性研究[D];第三軍醫(yī)大學(xué);2007年

4 梁艷;分泌型IgA在IgA腎病發(fā)病中的作用及機(jī)制研究[D];鄭州大學(xué);2015年

相關(guān)碩士學(xué)位論文 前10條

1 陳瀑;母乳SIgA抗感染作用的研究[D];重慶醫(yī)科大學(xué);2007年

2 李寒;顳下頜關(guān)節(jié)紊亂病患者心理因素與唾液SIgA的相關(guān)關(guān)系研究[D];天津醫(yī)科大學(xué);2013年

3 王文強(qiáng);抗雞SIgA單克隆抗體雜交瘤細(xì)胞株的建立[D];河南科技大學(xué);2010年

4 王曉東;急性肝內(nèi)膽汁淤積兔血清、膽汁及腸液中SIgA的變化及意義[D];華中科技大學(xué);2006年

5 李廷天;慢性阻塞性肺疾病及糖尿病大鼠肺泡灌洗液SIgA的含量測(cè)定[D];山東大學(xué);2011年

6 徐亞平;白介素Ⅱ?qū)淌茧u消化器官SIgA表達(dá)影響的研究[D];河南農(nóng)業(yè)大學(xué);2006年

7 全明輝;夏訓(xùn)對(duì)游泳運(yùn)動(dòng)員唾液sIgA影響及其與疲勞、免疫指標(biāo)相關(guān)性研究[D];華東師范大學(xué);2008年

8 羅樹(shù)立;盲升結(jié)腸可控膀胱術(shù)后尿sIgA含量研究[D];延邊大學(xué);2007年

9 王艷;唾液sIgA納米免疫生物傳感器的實(shí)驗(yàn)研究[D];重慶醫(yī)科大學(xué);2011年

10 朱鈺;IL-21，地塞米松，，苯甲酸雌二醇對(duì)小鼠SIgA形成的影響[D];重慶醫(yī)科大學(xué);2012年

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