本文選題：日本血吸蟲 + GST疫苗��； 參考：《華中科技大學(xué)》2010年博士論文

【摘要】： 寄生蟲能逃避宿主的免疫攻擊而繼續(xù)生存的現(xiàn)象稱為免疫逃避,其機理為分子模擬與偽裝、封閉抗體的產(chǎn)生等多種方式逃避宿主的體液和細胞免疫攻擊,因而寄生蟲能在宿主體內(nèi)長期存在并引起慢性感染。新近證實,調(diào)節(jié)性T細胞與寄生蟲逃避宿主免疫攻擊有關(guān),即“病原體可能會利用調(diào)節(jié)性T細胞當(dāng)做逃生的窗口”,如利什曼原蟲感染部位聚集了大量的調(diào)節(jié)性T細胞而有利于原蟲的存活,若用抗體阻斷調(diào)節(jié)性T細胞則有利于機體清除原蟲。 調(diào)節(jié)性T細胞最早于1995年由Sakaguchi等描述,主要包括自然性和誘導(dǎo)性調(diào)節(jié)性T細胞兩種類型。誘導(dǎo)性調(diào)節(jié)性T細胞由外來抗原誘導(dǎo)產(chǎn)生,自然性調(diào)節(jié)性T細胞即CD4+CD25+調(diào)節(jié)性T細胞,來源于胸腺并維持于外周,組成性表達CD25、Foxp3、CTLA-4和GITR等分子。CD25分子即IL-2受體的α鏈,對于維持調(diào)節(jié)性T細胞增殖及功能具有重要作用,但CD25分子同時也表達于活化的效應(yīng)細胞表面,因而不具有特異性。Foxp3為核轉(zhuǎn)錄因子,是調(diào)節(jié)性T細胞的特征性標志。CTLA-4(細胞毒性T淋巴細胞相關(guān)抗原4)是一種共抑制性受體,CTLA-4與機體的免疫耐受功能相關(guān)。CD4+CD25+調(diào)節(jié)性T細胞能抑制CD4+和CD8+效應(yīng)T細胞的激活,其抑制功能是由調(diào)節(jié)性T細胞與效應(yīng)細胞之間直接接觸或者由調(diào)節(jié)性T細胞分泌抑制性細胞因子IL-10和TGF-β來實現(xiàn)的,單獨及聯(lián)合使用相應(yīng)的阻斷性抗體有利于機體清除寄生蟲感染。 日本血吸蟲疫苗的研究經(jīng)歷了死疫苗、減毒活疫苗、基因工程疫苗和核酸疫苗的漫長過程,仍未取得較好的效果。WHO推薦的六種候選疫苗包括谷胱苷肽S轉(zhuǎn)移酶均不能穩(wěn)定地獲得40%以上的保護力。既然CD4+CD25+調(diào)節(jié)性T細胞能抑制效應(yīng)T細胞反應(yīng),因此推測日本血吸蟲在宿主體內(nèi)免疫逃避及日本血吸蟲疫苗的免疫保護性效果不佳均可能與調(diào)節(jié)性T細胞有關(guān)。 本文一方面探討了日本血吸蟲感染與調(diào)節(jié)性T細胞之間的關(guān)系,采用相應(yīng)抗體阻斷調(diào)節(jié)性T細胞,觀察其對機體清除日本血吸蟲感染能力的影響及其作用機制。另一方面探討了日本血吸蟲疫苗與調(diào)節(jié)性T細胞之間的關(guān)系,采用相應(yīng)抗體阻斷調(diào)節(jié)性T細胞觀察其對日本血吸蟲疫苗免疫保護性效果的影響及其作用機制。 本課題分為以下二個部分： 一、CD4+CD25+ Tregs在日本血吸蟲免疫逃避中的作用及其機制研究 目的：通過觀察日本血吸蟲感染對CD4+CD25+ Tregs的影響及使用anti-CD25 mAb對CD4+CD25+ Tregs的影響,了解CD4+CD25+ Tregs在日本血吸蟲免疫逃避中的作用及其機制。 方法：動物實驗分為三個部分 第一部分6～8周齡雌性BALB/c小鼠隨機分成二組,即正常對照組和感染組,感染組每只小鼠感染日本血吸蟲尾蚴40條,分別在感染后2周、3周、4周和5周剖殺小鼠,流式細胞術(shù)檢測各組小鼠脾淋巴細胞中CD4+CD25+ Tregs的比例。 第二部分6-8周齡雌性BALB／c小鼠隨機分成二組,即正常對照組和anti-CD25 mAb組,抗體組腹腔注射300μg anti-CD25 mAb,對照組注射等體積的PBS,使用抗體后2周剖殺小鼠,無菌取脾,制備單個脾淋巴細胞懸液,流式細胞術(shù)檢測各組小鼠脾淋巴細胞中CD4+CD25+ Tregs百分比。 第三部分6-8周齡雌性BALB/c小鼠隨機分成二組,即感染對照組和anti-CD25 mAb組。每只小鼠感染日本血吸蟲尾蚴40條,感染后2周,抗體使用組每只小鼠腹腔注射300μg anti-CD25 mAb,感染對照組注射等體積的PBS。感染后6周剖殺各組小鼠。計數(shù)蟲荷和每克肝臟內(nèi)蟲卵數(shù),計算減蟲率和每克肝臟組織中減卵率。無菌取各組小鼠脾臟,制備單個脾淋巴細胞懸液,收集脾細胞培養(yǎng)上清,夾心ELISA法檢測脾細胞上清中細胞因子含量。 結(jié)果： 1)日本血吸蟲感染后2周、3周、4周和5周,小鼠脾淋巴細胞中CD4+CD25+ Tregs百分比由感染前的1.99±0.10%分別上升至2.36±0.37%、2.8±0.05%、2.35±0.09%和2.68±0.05%。提示日本血吸蟲感染可誘導(dǎo)機體CD4+CD25+ Tregs升高。 2)正常對照組小鼠脾淋巴細胞中CD4+CD25+ Tregs百分比平均值為1.99±0.10%,使用anti-CD25 mAb后2周百分比平均值為0.20±0.05%,抗體組明顯低于對照組(P0.01)。提示anti-CD25 mAb可部分阻斷CD4+CD25+ Tregs。 3)使用anti-CD25 mAb組小鼠蟲荷較未使用抗體組減少18.99%,每克肝臟蟲卵數(shù)減少15.86%。提示CD4+CD25+ Tregs下降有利于宿主對血吸蟲的清除。 4)使用anti-CD25 mAb組小鼠脾細胞培養(yǎng)上清中細胞因子IFN-γ,、IL-5明顯高于感染對照組。 結(jié)論：Anti-CD25 mAb能部分阻斷CD4+CD25+ Tregs,使用后有利于機體清除日本血吸蟲。 二、CD4+CD25+ Tregs對日本血吸蟲GST疫苗保護性效果的影響及其作用機制 目的：通過觀察日本吸蟲GST疫苗對CD4+CD25+ Tregs的影響及anti-CD25 mAb對CD4+CD25+ Tregs表達的影響,探討CD4+CD25+ Tregs對GST疫苗免疫保護效果的影響及其作用機制。 方法：雌性BALB／c小鼠隨機分成五組,正常組、感染對照組、anti-CD25 mAb組、GST組以及anti-CD25 mAb與GST聯(lián)合組。GST組和聯(lián)合組小鼠背部皮下多點注射日本血吸蟲GST疫苗50μg/鼠,每次間隔2周,共免疫三次,末次免疫后2周,每只小鼠感染日本血吸蟲尾蚴40條,感染后2周,anti-CD25 mAb組和聯(lián)合組小鼠腹腔注射anti-CD25 mAb 300μg/鼠,對照組注射等體積的PBS。分別在感染后2周、3周、4周和5周剖殺四組小鼠。無菌取各組小鼠脾臟,制備單個脾淋巴細胞懸液,流式細胞術(shù)檢測脾淋巴細胞中CD4+CD25+ Tregs百分比；收集脾細胞培養(yǎng)上清,夾心ELISA法檢測脾細胞培養(yǎng)上清中細胞因子含量。感染后5周剖殺的小鼠同時計數(shù)蟲荷和每克肝臟蟲卵數(shù),計算減蟲率和每克肝組織中減卵率。小鼠肝組織石蠟切片HE染色,觀察各組小鼠蟲卵肉芽腫的變化。 結(jié)果： 1)日本血吸蟲感染后2周,感染對照組與GST組脾淋巴細胞中CD4+CD25+ Tregs百分比平均值分別為2.36±0.37%和3.36±0.06%；感染后3周,其百分比平均值分別為2.8±0.05%和2.97±0.08%；感染后4周,其百分比平均值分別為2.35±0.09%和2.47±0.09%；感染后5周,其百分比平均值分別為2.68±0.05%和3.03±±0.13%。提示GST疫苗能誘導(dǎo)機體CD4+CD25+ Tregs升高。 2)使用anti-CD25 mAb后1周(即感染后3周),感染對照組與anti-CD25 mAb組小鼠脾淋巴細胞中CD4+CD25+ Tregs百分比平均值分別為2.8±0.05%和0.13±0.04%；使用anti-CD25 mAb后2周(即感染后4周),百分比平均值分別為2.35±0.09%和0.9±0.23%；使用anti-CD25 mAb后3周(即感染后5周),百分比平均值分別為2.68±0.05%和1.93±0.03%。提示使用anti-CD25 mAb后1周能部分封閉CD4+CD25+ Tregs,使用anti-CD25 mAb后2周、3周其百分比逐漸上升,但仍明顯低于感染對照組。 3)GST組小鼠對日本血吸蟲減蟲率及減卵率分別為24.98%和32%,而GST與anti-CD25 mAb聯(lián)合組減蟲率及減卵率分別為43.43%和49%。提示anti-CD25 mAb可作為佐劑增強GST疫苗的保護性效果。 4)日本血吸蟲感染早期以Thl型免疫反應(yīng)為主,感染后4周雌蟲排卵后以Th2型免疫反應(yīng)為主,而使用anti-CD25 mAb后Th1型細胞因子IFN-y仍維持在較高水平,有利于機體清除日本血吸蟲。提示anti-CD25 mAb增強GST疫苗免疫保護性效果的機制為增強機體內(nèi)Thl型免疫反應(yīng)。 5)病理組織學(xué)檢查顯示各感染組單個蟲卵肉芽腫直徑及浸潤細胞無明顯差異。提示anti-CD25 mAb未明顯增強小鼠肝臟蟲卵肉芽腫的病理變化。 結(jié)論：日本血吸蟲GST疫苗能誘導(dǎo)CD4+CD25+ Tregs比例上升,因而會影響GST疫苗的保護性效果；anti-CD25 mAb能部分阻斷CD4+CD25+ Tregs,同時增強Thl型免疫反應(yīng),因而能提高GST疫苗的免疫保護性效果,因此anti-CD25 mAb能作為佐劑增強GST疫苗的保護性效果。 本研究結(jié)論如下： 1)寄生蟲的免疫逃避與CD4+CD25+ Tregs有關(guān),CD4+CD25+ Tregs升高有利于血吸蟲逃避宿主的免疫攻擊。 2)首次證明日本血吸蟲GST疫苗的保護性效果與宿主的CD4+CD25+ Tregs有關(guān),GST疫苗在感染背景下能誘導(dǎo)小鼠脾淋巴細胞中CD4+CD25+ Tregs升高,從而影響GST疫苗的保護性效果。 3)首次證明anti-CD25 mAb可增強日本血吸蟲GST疫苗的保護性效果,其作用機制是通過阻斷CD4+CD25+ Tregs和增強Thl型免疫反應(yīng)來實現(xiàn)的。 4)首次提出anti-CD25 mAb可作為佐劑用來增強日本血吸蟲GST疫苗的保護性效果。
[Abstract]:Parasites can escape the host's immune attacks and continue to survive the phenomenon known as immune escape, its mechanism is a variety of ways to escape the host's humoral and cellular immune attacks, such as molecular simulation and camouflage, the production of closed antibodies and so on. Thus parasites can exist in the host for a long time and cause chronic infection. Recently, regulatory T cells are newly confirmed to be sent to the host. The parasite escapes from the host immune attack, that is, "pathogens may use regulatory T cells as escape windows", such as Leishmania infecting sites that accumulate a large number of regulatory T cells to help protozoa survival. If the antibodies are used to block regulatory T cells, it is beneficial to remove the protozoa.
As early as in 1995, regulatory T cells were described by Sakaguchi, including two types of natural and inducible regulatory T cells. Inducible regulatory T cells were induced by external antigens, and natural regulatory T cells, CD4+CD25+ regulated T cells, derived from the thymus and maintained in the peripheral, expressed CD25, Foxp3, CTLA-4 and GITR, and so on. The molecular.CD25 molecule, the alpha chain of the IL-2 receptor, plays an important role in maintaining the proliferation and function of regulatory T cells, but the CD25 molecule is also expressed on the activated cell surface, so it does not have specific.Foxp3 as a nuclear transcription factor, and is a characteristic marker of the regulatory T cell.CTLA-4 (cytotoxic T lymphocyte associated antigen 4). Co suppressor receptor, CTLA-4 and the immune tolerance function of the body,.CD4+CD25+ regulatory T cells can inhibit the activation of CD4+ and CD8+ effect T cells. The inhibitory function is achieved by direct contact between regulatory T cells and effector cells or by the secretion of inhibitory cytokine IL-10 and TGF- beta by regulatory T cells, alone and in combination. The use of corresponding blocking antibodies is beneficial to the elimination of parasitic infections.
The study of Schistosoma japonicum vaccine has experienced a long process of dead vaccine, live attenuated vaccine, genetic engineering vaccine and nucleic acid vaccine. The six candidate vaccines recommended by.WHO, including glutathione S transferase, are not stable to obtain more than 40% protection. Both CD4+CD25+ regulatory T cells can inhibit the effect of T cells Therefore, it is speculated that the immune escape of Schistosoma japonicum in vivo and the poor protective effect of Schistosoma japonicum vaccine may be related to regulatory T cells.
On the one hand, the relationship between Schistosoma japonicum infection and regulatory T cells was discussed, and the corresponding antibodies were used to block regulatory T cells to observe the effect and mechanism of its effect on the organism's ability to scavenging Schistosoma japonicum infection. On the other hand, the relationship between Schistosoma japonicum vaccine and regulatory T cells was discussed, and the corresponding antibody resistance was used. The effects of T cells on the protective effect of Schistosoma japonicum vaccine were observed.
This topic is divided into the following two parts:
The role and mechanism of CD4+CD25+ Tregs in immune escape of Schistosoma japonicum
Objective: to understand the role and mechanism of CD4+CD25+ Tregs in immune evasion of Schistosoma japonicum by observing the effect of Schistosoma japonicum infection on CD4+CD25+ Tregs and the effect of anti-CD25 mAb on CD4+CD25+ Tregs.
Methods: the animal experiment was divided into three parts
The first part of the 6~8 week old female BALB/c mice was randomly divided into two groups, that is, the normal control group and the infection group. The infected group infected 40 Schistosoma japonicum cercariae in each mouse. The mice were killed at 2 weeks, 3 weeks, 4 and 5 weeks after infection, and the proportion of CD4+CD25+ Tregs in the splenocytes of each group was detected by flow cytometry.
The second part of the 6-8 week old female BALB / c mice were randomly divided into two groups, namely the normal control group and the anti-CD25 mAb group. The antibody group was intraperitoneally injected with 300 mu g anti-CD25 mAb, the control group was injected with equal volume PBS, the mice were killed for 2 weeks after using the antibody, the spleen was taken asepsis, the single splenic lymphocyte suspension was prepared, and the splenic lymphocytes of each group were detected by flow cytometry. Percentage of medium CD4+CD25+ Tregs.
Third parts of the 6-8 week old female BALB/c mice were randomly divided into two groups, namely, infection control group and anti-CD25 mAb group. Each mouse infected with 40 Schistosoma japonicum cercariae and 2 weeks after infection. The antibody group was injected with 300 g anti-CD25 mAb in each mouse, infected with the same volume of PBS. infection in the control group for 6 weeks after 6 weeks. The number of eggs in each gram of liver, the rate of worm reduction and the rate of egg reduction in every gram of liver were calculated. The spleen of mice in each group was taken asepsis, the single splenic lymphocyte suspension was prepared, the splenocyte culture supernatant was collected, and the content of cytokines in the splenocyte supernatant was detected by the sandwich ELISA method.
Result:
1) 2 weeks, 3 weeks, 4 weeks and 5 weeks after Schistosoma japonicum infection, the percentage of CD4+CD25+ Tregs in spleen lymphocytes of mice increased from 1.99 + 0.10% before infection to 2.36 + 0.37%, 2.8 + 0.05%, 2.35 + 0.09% and 2.68 + 0.05%., suggesting that the infection of Schistosoma japonicum could induce the increase of CD4+CD25+ Tregs in the body.
2) the average value of CD4+CD25+ Tregs in spleen lymphocyte in normal control group was 1.99 + 0.10%, and the average value of 2 weeks after using anti-CD25 mAb was 0.20 + 0.05%, and the antibody group was significantly lower than that of the control group (P0.01). It suggested that anti-CD25 mAb could partially block CD4+CD25+ Tregs..
3) the decrease of the number of mice in the anti-CD25 mAb group was 18.99% less than that in the unused antibody group. The decrease of the number of eggs per gram of liver 15.86%. suggests that the decrease of CD4+CD25+ Tregs is beneficial to the host's clearance of Schistosoma.
4) using anti-CD25 mAb group, the cytokine IFN- gamma in spleen cell culture supernatant of mice was significantly higher than that of infection control group (IL-5).
Conclusion: Anti-CD25 mAb can partially block CD4+CD25+ Tregs, which is beneficial to the elimination of Schistosoma japonicum.
Two, the protective effect of CD4+CD25+ Tregs on Schistosoma japonicum GST vaccine and its mechanism.
Objective: To investigate the effect of anti-CD25 mAb on the expression of CD4+CD25+ Tregs by observing the effect of GST vaccine on CD4+CD25+ Tregs and the effect of anti-CD25 mAb on the expression of CD4+CD25+ Tregs, and to explore the effect of CD4+CD25+ Tregs on the protective effect of GST vaccine and its mechanism.
Methods: female BALB / c mice were randomly divided into five groups, the normal group, the infection control group, the anti-CD25 mAb group, the GST group and the anti-CD25 mAb and GST combined group.GST group and the combined group of mice with the back subcutaneous injection of the 50 mu g/ rat of Schistosoma japonicum GST vaccine for 2 weeks each time, three times and 2 weeks after the last immunization, each mouse infected with the Japanese blood sucking. 40 strains of cercariae, 2 weeks after infection, the anti-CD25 mAb group and the combined group of mice were intraperitoneally injected with anti-CD25 mAb 300 mu g/ rats, and the PBS. in the control group was killed in 2 weeks, 3 weeks, 4 weeks and 5 weeks after infection. The spleen of the mice was taken asepsis to prepare the single splenocytes suspension, and the flow cytometry was used to detect the CD4+CD25+ in the spleen lymphocyte. The percentage of Tregs, splenocyte culture supernatant was collected and sandwich ELISA method was used to detect the cytokine content in the supernatant of splenocyte culture. In the 5 weeks after infection, the mice were counted and the number of eggs per gram of liver were counted. The rate of worm reduction and the rate of egg reduction in each gram of liver were calculated. The mouse liver tissue was stained with paraffin slice HE, and the granuloma of eggs was observed in mice in each group. Change.
Result:
1) for 2 weeks after Schistosoma japonicum infection, the average percentage of CD4+CD25+ Tregs in the spleen lymphocytes of the infected control group and the GST group was 2.36 + 0.37% and 3.36 + 0.06% respectively. The average percentage of the percentage was 2.8 + 0.05% and 2.97 +, respectively 3 weeks after the infection, and the average percentage of the infection after infection was 2.35 + 0.09% and 0.06%. The average percentages were 2.68 + 0.05% and 3.03 + 0.13%. respectively, suggesting that GST vaccine can induce CD4+CD25+ Tregs elevation.
2) the average value of CD4+CD25+ Tregs percentage in the spleen lymphocytes of the infected control group and the anti-CD25 mAb group was 2.8 + 0.05% and 0.13 + 0.04%, respectively after the use of anti-CD25 mAb after 1 weeks of infection, and the average value of the percentage was 2.35 + 0.09% and 0.9 + 0.23% in the 2 weeks after the use of anti-CD25 mAb (i.e., 4 weeks after infection). (5 weeks after infection), the percentage averages were 2.68 + 0.05% and 1.93 + 0.03%., respectively, indicating that CD4+CD25+ Tregs could be partially closed for 1 weeks after anti-CD25 mAb. The percentage of anti-CD25 mAb increased gradually in the 2 weeks and 3 weeks after the use of mAb, but it was still significantly lower than that in the infection control group.
3) the rate of worm reduction and egg reduction of Schistosoma japonicum in GST group were 24.98% and 32% respectively, while the rate of worm reduction and the rate of egg reduction in the combination group of GST and anti-CD25 mAb were 43.43% and 49%., respectively, suggesting that anti-CD25 mAb could be used as an adjuvant to enhance the protective effect of GST vaccine.
4) the early infection of Schistosoma japonicum was dominated by Thl type immune response. After 4 weeks of infection, the female parasite was dominated by Th2 type immune response. After anti-CD25 mAb, the Th1 cytokine IFN-y remained at a high level, which was beneficial to the organism to remove the Schistosoma japonicum. The mechanism of anti-CD25 mAb to strengthen the immune protective effect of GST vaccine was the enhancement mechanism Type Thl immune response in the body.
5) histopathological examination showed that there was no significant difference between the diameter of single egg granuloma and infiltrating cells in each infection group. It was suggested that anti-CD25 mAb did not significantly enhance the pathological changes of egg granuloma in the liver of mice.
Conclusion: the GST vaccine of Schistosoma japonicum can induce the increase in the proportion of CD4+CD25+ Tregs and thus affect the protective effect of the GST vaccine. Anti-CD25 mAb can partially block the CD4+CD25+ Tregs and enhance the Thl type immune response, so it can improve the protective effect of the GST vaccine. Therefore, anti-CD25 mAb can be used as an adjuvant to enhance the protection of the vaccine. Sexual effect.
The conclusions of this study are as follows:
1) the immune evasion of parasites is related to CD4+CD25+ Tregs, and the increase of CD4+CD25+ Tregs is beneficial for schistosomiasis to evade the host's immune attack.
2) the protective effect of the GST vaccine of Schistosoma japonicum is related to the host's CD4+CD25+ Tregs for the first time. The GST vaccine can induce the increase of CD4+CD25+ Tregs in the spleen lymphocyte of mice in the infected background, thus affecting the protective effect of the GST vaccine.
3) it is the first time that anti-CD25 mAb can enhance the protective effect of GST vaccine of Schistosoma japonicum, and its mechanism is achieved by blocking the CD4+CD25+ Tregs and enhancing the Thl immune response.
4) for the first time, anti-CD25 mAb can be used as an adjuvant to enhance the protective effect of GST vaccine against Schistosoma japonicum.
【學(xué)位授予單位】：華中科技大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2010
【分類號】：R392

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