本文選題：同種異基因 + 凋亡細(xì)胞��； 參考：《南方醫(yī)科大學(xué)》2009年碩士論文

【摘要】： 目前,原位肝移植(Orthotopic liver transplantation,OLT)是治療終末期肝病最有效和常規(guī)措施。然而,盡管由于外科技術(shù)的標(biāo)準(zhǔn)化、免疫抑制劑的不斷研發(fā)和應(yīng)用,移植物的長(zhǎng)期存活率沒(méi)有明顯提高。器官移植術(shù)后的排斥反應(yīng)仍是威脅患者和移植物長(zhǎng)期存活的主要原因。免疫抑制劑的應(yīng)用,不僅使器官移植成為終末期腎、肝、心臟疾病可接受的治療方式,而且顯著減少了急性排斥的發(fā)生率,同時(shí)顯著提高了器官移植病人的短期、長(zhǎng)期生存率。然而,免疫抑制劑的應(yīng)用帶來(lái)了許多問(wèn)題。首先,要終身連續(xù)對(duì)免疫系統(tǒng)進(jìn)行非特異性免疫抑制。第二,當(dāng)前使用的免疫抑制劑中,沒(méi)有一種能完全預(yù)防急性排斥或者慢性排斥。第三,免疫抑制劑的應(yīng)用帶來(lái)了腫瘤和感染的風(fēng)險(xiǎn)。第四,免疫抑制劑的應(yīng)用增加了移植病人高血壓的風(fēng)險(xiǎn)以及由此導(dǎo)致的心血管并發(fā)癥。因此,誘導(dǎo)受者對(duì)供者器官特異性免疫耐受是解決排斥反應(yīng)最理想的措施,相對(duì)免疫抑制療法,誘導(dǎo)免疫耐受的優(yōu)勢(shì)是從根本上避免了排斥反應(yīng),又不影響機(jī)體的正�？垢腥竞兔庖弑O(jiān)視功能,同時(shí)避免了藥物毒性。而且,耐受的誘導(dǎo)對(duì)于最終克服異種移植免疫學(xué)障礙也許是最佳途徑,因?yàn)楫惙N移植免疫抑制需長(zhǎng)期高水平的、非特異性的免疫抑制劑來(lái)維持。因此,誘導(dǎo)移植免疫耐受性,控制移植物排斥反應(yīng),保護(hù)移植器官的功能,這無(wú)論在同種移植和異種移植中都是十分重要的課題。 由于移植免疫耐受的機(jī)制十分復(fù)雜,盡管誘導(dǎo)免疫耐受的方法眾多,但均未能達(dá)到完全可靠持久的特異性耐受。細(xì)胞凋亡是生物體內(nèi)普遍存在的一種生理和病理現(xiàn)象,是正常器官和組織發(fā)育、清除有害的、過(guò)量的和無(wú)功能細(xì)胞、維持自身穩(wěn)態(tài)的必要環(huán)節(jié)�，F(xiàn)有研究表明:凋亡是機(jī)體免疫狀態(tài)保持平衡和穩(wěn)定的重要作用機(jī)制,凋亡細(xì)胞對(duì)免疫系統(tǒng)存在著主動(dòng)的調(diào)節(jié)作用。凋亡細(xì)胞能分泌脂類趨化因子,改變自身胞膜結(jié)構(gòu)表達(dá)“eat-me”信號(hào),誘導(dǎo)吞噬細(xì)胞對(duì)其進(jìn)行清除;同時(shí)凋亡細(xì)胞被抗原提呈細(xì)胞吞噬后,通過(guò)吞噬細(xì)胞分泌抑制性免疫因子如TGF-β、PGE2、IL-10等,造成了特殊的抗原識(shí)別微環(huán)境,可以促使相關(guān)淋巴細(xì)胞針對(duì)凋亡抗原產(chǎn)生免疫耐受,而不會(huì)引起炎性免疫應(yīng)答。據(jù)此,孫爾維等提出利用供體凋亡細(xì)胞輸注受體誘導(dǎo)供體特異性免疫耐受的理論設(shè)想。 細(xì)胞因子是活化細(xì)胞產(chǎn)生的細(xì)胞間信號(hào)多肽。大多數(shù)細(xì)胞因子都有多種來(lái)源,多種作用靶位和多種功效。細(xì)胞因子網(wǎng)絡(luò)是參與免疫識(shí)別、應(yīng)答反應(yīng)的重要成分,也是決定免疫反應(yīng)發(fā)生方向的主要因素之一�？乖晕镔|(zhì)進(jìn)入機(jī)體后引起免疫系統(tǒng)發(fā)生的各種反應(yīng)變化中包括了細(xì)胞因子比例水平的改變,由于后者直接參與前者的發(fā)生過(guò)程與最后結(jié)果表現(xiàn),從而探討細(xì)胞因子的變現(xiàn)表現(xiàn)對(duì)分析以及預(yù)測(cè)免疫反應(yīng)發(fā)生和走向有一定的意義。 我們課題組以前的工作證實(shí),一定數(shù)量的供體凋亡脾淋巴細(xì)胞預(yù)輸注可以誘導(dǎo)大鼠心、肝臟移植模型產(chǎn)生特異性免疫耐受,延長(zhǎng)移植存活的時(shí)間。且通過(guò)對(duì)凋亡細(xì)胞進(jìn)行示蹤實(shí)驗(yàn),發(fā)現(xiàn)凋亡的脾淋巴細(xì)胞主要聚集并駐留于肝臟,且對(duì)肝臟組織的細(xì)胞因子的微環(huán)境產(chǎn)生了影響。但輸入的過(guò)程中是否也影響外周的細(xì)胞因子微環(huán)境,這對(duì)下部進(jìn)一步探討誘導(dǎo)凋亡的機(jī)制有重要的影響。所以本實(shí)驗(yàn)主要在前期的基礎(chǔ)上,對(duì)供體凋亡脾淋巴細(xì)胞預(yù)輸注是否影響外周血微環(huán)境進(jìn)行研究。 目的 已知凋亡細(xì)胞發(fā)生免疫調(diào)節(jié)作用時(shí)也會(huì)同時(shí)伴有細(xì)胞因子等微環(huán)境的變化。且前期工作證明供體凋亡脾淋巴細(xì)胞輸注對(duì)受體肝臟內(nèi)細(xì)胞因子微環(huán)境有影響,本部分對(duì)供體凋亡細(xì)胞輸注后對(duì)外周血免疫微環(huán)境中一系列重要細(xì)胞因子的變化進(jìn)行觀察,以了解供體凋亡脾淋巴細(xì)胞輸注對(duì)外周血細(xì)胞因子的影響。 方法 供體C57BL小鼠14只,8-10周,雄性;受體Balb/c小鼠6-8周,50只,雄性。具體如下: (1)機(jī)械研磨法分離脾臟細(xì)胞,易得分離液分離淋巴細(xì)胞。 (2)紫外線照射法誘導(dǎo)凋亡,流式細(xì)胞儀檢測(cè)細(xì)胞凋亡率。 (3)采用尾靜脈輸入法,每處理組每時(shí)間點(diǎn)5只小鼠,預(yù)輸注處理分組:供體脾臟活細(xì)胞處理組(Liver cell treatment group,LG),供體脾臟凋亡細(xì)胞處理組(Apoptotic cell treatment group,AG); (4)檢測(cè)時(shí)間點(diǎn):輸注后0h、1h、3h、6h、12h; (5)采用體外心臟采血法,收集樣本; (6) Luminex技術(shù)液態(tài)芯片法檢測(cè)外周血IL-1β、IL-2、IL-4、IL-5、IL-6、IL-10、IL-12、GM-CSF(粒細(xì)胞-巨細(xì)胞激落刺激因子)、IFN-γ、TNF(腫瘤壞死因子); (7)所有實(shí)驗(yàn)數(shù)據(jù)利用SPSS13.0和GraphPad PRISM 3.02等軟件進(jìn)行統(tǒng)計(jì)學(xué)分析和作圖。 統(tǒng)計(jì) ①兩因素對(duì)各因子作用的分析比較,使用SPSS13.0軟件之General LinearModel-Univatiate分析,兩處理組各個(gè)點(diǎn)的比較,使用SPSS13.0軟件之One-way ANOVE分析,方差不齊的,選用Independent Samples近似Test; ②各個(gè)處理組中時(shí)間點(diǎn)于0h之間的比較,使用SPSS13.0軟件之One-way ANOVE分析,方差不齊的,選用Independent Samples近似Test; ③采用GraphPad PRISM 3.02軟件進(jìn)行制圖。 結(jié)果 (1)流式細(xì)胞術(shù)分析,紫外線誘導(dǎo)的凋亡細(xì)胞的比例可達(dá)到41.07%以上。 (2)活細(xì)胞組對(duì)外周細(xì)胞因子的影響(因IL-1β、IL-2、IL-4、IL-5、TNF在外周血液中的水平低于儀器的檢測(cè)水平,未測(cè)出):外周血中IFN-γ在6h時(shí)細(xì)胞因子濃度明顯升高(P=0.010,6h),IL-10于3h和6h時(shí)細(xì)胞因子濃度明顯升高(P=0.009,3h;P=0.015,6h),IL-12、GM-CSF、IFN-γ在各個(gè)時(shí)間點(diǎn)無(wú)顯著性差異。 (3)凋亡細(xì)胞組對(duì)外周細(xì)胞因子的影響:IL-6、IL-10、IL-12、IFN-γ在各個(gè)時(shí)間點(diǎn)無(wú)明顯的差異,GM-CSF在3h時(shí)明顯升高(P=0.049)。 (4)處理組不同對(duì)外周細(xì)胞因子微環(huán)境的影響: ①IL-6:活細(xì)胞組和凋亡細(xì)胞組相比于1h時(shí)存在顯著性差異(P=0.035,1h),活細(xì)胞組的水平高于凋亡細(xì)胞組。 ②IL-10:活細(xì)胞組和凋亡細(xì)胞組相比于分別于3h、6h、12時(shí)存在顯著性差異(P=0.001,3h;P=0.001,6h;P=0.043,12h),活細(xì)胞組的水平高于凋亡細(xì)胞組。 ③IL-12、GM-CSF、IFN-γ在活細(xì)胞組和凋亡細(xì)胞組相比中無(wú)顯著性差異。 結(jié)論 本實(shí)驗(yàn)證明凋亡細(xì)胞組和活細(xì)胞組相比,外周IL-6在1h時(shí)有顯著性差異和IL-10在3h、6h和12h時(shí)存在顯著性差異,活細(xì)胞組高于凋亡細(xì)胞組,其他細(xì)胞因子都無(wú)顯著性差異,而且活細(xì)胞輸注后,3h、6h的IL-10濃度明顯高于0h。凋亡細(xì)胞輸注后對(duì)細(xì)胞因子基本無(wú)改變,從IL-6和IL-10的結(jié)果我們可以推測(cè):活細(xì)胞輸注后,機(jī)體產(chǎn)生了急性炎性反應(yīng),使IL-6于1h時(shí)升高,而3小時(shí)后,機(jī)體為了避免炎性反應(yīng)過(guò)度而采取了保護(hù)措施,增加IL-10的分泌,阻斷了單核、巨噬細(xì)胞合成IL-6、TNFα等介質(zhì),而凋亡細(xì)胞對(duì)機(jī)體外周血無(wú)明顯的作用,根據(jù)凋亡細(xì)胞是一種死細(xì)胞,具有完整的包膜,在組織中的清理主要為吞噬作用,可能相對(duì)于異種的活細(xì)胞引起的炎性反應(yīng)作用較弱。凋亡細(xì)胞輸入后,對(duì)外周血中GM-CFS濃度在3h時(shí)明顯升高和活細(xì)胞輸入后,6h時(shí)對(duì)外周血中IFN-γ濃度的影響有顯著性意義,具體機(jī)制還需要進(jìn)一步研究。而根據(jù)以往的研究,凋亡細(xì)胞對(duì)機(jī)體有明確的作用,可以引起免疫耐受的,而且本課題組的前期研究通過(guò)對(duì)凋亡細(xì)胞進(jìn)行示蹤實(shí)驗(yàn),發(fā)現(xiàn)凋亡的脾淋巴細(xì)胞主要聚集并駐留于肝臟,且對(duì)肝臟組織的細(xì)胞因子的微環(huán)境產(chǎn)生了影響,包括IL-1β、IL-4、IL-10、和IFN-γ的特異性分泌水平提高,從而推測(cè)凋亡細(xì)胞主要在在肝臟起作用,對(duì)外周無(wú)明顯的影響。但具體的機(jī)制還需要進(jìn)一步對(duì)肝組織中其他細(xì)胞類型和反應(yīng)功能的改變,如記憶T細(xì)胞、B細(xì)胞等進(jìn)行相續(xù)的研究。
[Abstract]:At present, Orthotopic liver transplantation (OLT) is the most effective and conventional measure for the treatment of end-stage liver disease. However, despite the standardization of surgical techniques and the continuous development and application of immunosuppressive agents, the long-term survival rate of the graft is not significantly improved. The rejection after organ transplantation is still a threat to patients and transplant. The main cause of long term survival. The application of immunosuppressive agents not only makes organ transplantation an acceptable treatment for end-stage kidney, liver and heart disease, but also significantly reduces the incidence of acute rejection, and significantly improves the short-term and long-term survival rate of organ transplant patients. However, the application of immunosuppressive agents has brought many questions. Second, none of the immunosuppressants currently used can completely prevent acute rejection or chronic rejection. Third, the application of immunosuppressants brings the risk of cancer and infection. Fourth, the application of immunosuppressive agents increases the hypertension of transplant patients. Therefore, it is the most ideal measure to induce the recipient's organ specific immune tolerance to the rejection reaction. Relative immunosuppressive therapy, the advantage of inducing immune tolerance is to avoid the rejection, and do not affect the normal anti infection and immune surveillance function of the body. Moreover, tolerance induction may be the best way to eventually overcome xenotransplantation immunological barriers, because xenograft immunosuppression needs long-term high levels of non specific immunosuppressive agents to maintain. Therefore, it induces transplant immune tolerance, controls graft rejection, and protects the function of transplant organs. It is a very important topic both in homologous transplantation and xenotransplantation.
The mechanism of transplantation immune tolerance is very complex. Although there are many methods to induce immune tolerance, they are not fully reliable and persistent. Apoptosis is a common physiological and pathological phenomenon in the organism. It is normal organ and tissue development, detrimental, excessive and non functional cells, and maintains itself. The necessary link of steady state. The existing research shows that apoptosis is an important mechanism for the balance and stability of the immune state of the body. Apoptotic cells have the active regulation effect on the immune system. Apoptotic cells can secrete chemotactic factors of lipid, change their membrane structure to express "eat-me" signals, induce phagocytes to scavenging them. When the apoptotic cells were phagocyted by antigen presenting cells and secreted by phagocytic cells such as TGF- beta, PGE2, IL-10 and so on, the specific antigen recognition microenvironment was created, which could induce the related lymphocyte to produce immune tolerance against the apoptotic antigen, without causing inflammatory response. Accordingly, sun Erwei and so on proposed the use of donor apoptosis. A theoretical assumption of donor specific immune tolerance induced by cell infusion receptors.
Cytokine is an intercellular signal polypeptide produced by activated cells. Most of the cytokines have a variety of sources, multiple targets and many functions. Cytokine network is an important component of immune recognition, response response and one of the main factors that determine the direction of the immune response. Antigenic substances are induced to escape from the body. The changes in the various responses of the Phytophthora system include changes in the proportion of cytokines, as the latter directly participates in the process of the former and the performance of the final results, thus exploring the expression of cytokine in the analysis and prediction of the occurrence and direction of the immune response.
The previous work of our group confirmed that a certain number of donor apoptotic splenic lymphocytes pretransfused can induce rat heart, the liver transplantation model produces specific immune tolerance and prolongs the survival time of the transplanted cells. And the apoptotic cells are traced by the apoptotic cells, and the apoptotic splenic lymphocytes mainly gather and reside in the liver. The microenvironment of cytokine in the dirty tissue has an impact. But whether the input process also affects the peripheral cytokine microenvironment, which has an important influence on the mechanism of inducing apoptosis in the lower part. Therefore, this experiment is mainly on the basis of the early stage to affect the peripheral blood microenvironment of donor apoptosis of splenic lymphocytic cells. Research.
objective
It is known that the immunoregulation of apoptotic cells may also be accompanied by changes in the microenvironment such as cytokine, and the earlier work has proved that the donor apoptotic splenic lymphocyte infusion has an effect on the cell factor microenvironment in the recipient liver. This part is a series of important cytokines in the peripheral blood immune microenvironment after the donor apoptotic cells are transfused. Changes were observed in order to understand the effects of donor apoptotic splenic lymphocyte infusion on peripheral blood cytokines.
Method
The donor C57BL mice were 14, 8-10 weeks, male, recipient Balb/c mice 6-8 weeks, 50 male, as follows:
(1) the splenic cells were separated by mechanical attrition, and the lymphocytes were separated easily.
(2) apoptosis was induced by ultraviolet irradiation, and apoptosis rate was detected by flow cytometry.
(3) using the tail vein input method, 5 mice per time point per treatment group, pre infusion treatment group: donor spleen living cell treatment group (Liver cell treatment group, LG), donor spleen apoptotic cell processing group (Apoptotic cell treatment group, AG);
(4) detection time points: 0h, 1H, 3h, 6h, 12h after infusion;
(5) in vitro cardiac blood sampling was used to collect samples.
(6) Luminex technique was used to detect peripheral blood IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, GM-CSF (granulocyte - cytomegalocell irritation factor), IFN- gamma, TNF (tumor necrosis factor);
(7) all experimental data were statistically analyzed and plotted using SPSS13.0 and GraphPad PRISM 3.02 software.
Statistics
(1) the analysis and comparison of the two factors on the role of each factor, using the General LinearModel-Univatiate analysis of SPSS13.0 software, the comparison of each point in the two treatment group, the One-way ANOVE analysis of the SPSS13.0 software, the variance of the variance, and the selection of Independent Samples to approximate Test;
(2) the comparison of the time points between 0h in each treatment group, using the One-way ANOVE analysis of SPSS13.0 software, and using the Independent Samples approximation Test as the variance is uneven.
(3) using GraphPad PRISM 3.02 software for drawing.
Result
(1) flow cytometry analysis showed that the proportion of apoptotic cells induced by UV could reach more than 41.07%.
(2) the influence of the peripheral cytokine in the living cell group (IL-1 beta, IL-2, IL-4, IL-5, TNF in the peripheral blood is lower than the instrument detection level, not measured): the concentration of cytokine in the peripheral blood of IFN- gamma in 6h is significantly increased (P=0.010,6h) and IL-10 at 3H and 6h. There is no significant difference between gamma at all time points.
(3) the effect of apoptotic cell group on peripheral cytokines: IL-6, IL-10, IL-12 and IFN- gamma were not significantly different at all time points, and GM-CSF increased significantly at 3H (P=0.049).
(4) the effect of treatment group on peripheral cytokine microenvironment:
There was significant difference between IL-6: living cell group and apoptotic cell group when compared with 1H (P=0.035,1h), and the level of living cell group was higher than that of apoptotic cell group.
2. There were significant differences between the IL-10: living cell group and the apoptotic cell group at 3h, 6h, and 12 (P=0.001,3h; P=0.001,6h; P=0.043,12h). The level of the living cell group was higher than that of the apoptotic cell group.
There was no significant difference in IL-12, GM-CSF and IFN- gamma between the living cell group and the apoptotic cell group.
conclusion
This experiment showed that the apoptotic cell group and the living cell group had significant difference in the peripheral IL-6 at 1H and the significant difference between the IL-10 in 3h, 6h and 12h. The living cell group was higher than the apoptotic cell group, and there was no significant difference in the other cytokines. Moreover, the IL-10 concentration of 3H and 6h was significantly higher than that of the apoptotic cells after the transfusing of the living cells. The factors are basically unchanged. From the results of IL-6 and IL-10, we can speculate that after the infusion of living cells, the body produces an acute inflammatory response, which raises the IL-6 at 1H, and 3 hours later, the body has taken protective measures to avoid excessive inflammatory response, increased the secretion of IL-10, blocked the mononuclear, and macrophages synthesized IL-6, TNF A and other mediators, and apoptosis The cells have no obvious effect on the peripheral blood of the body. According to the apoptotic cells, a dead cell is a dead cell, with a complete capsule. The cleaning in the tissue is mainly phagocytosis, which may be weaker than that of the xenogeneic living cells. After the input of the apoptotic cells, the concentration of GM-CFS in the peripheral blood is obviously elevated at 3H and the input of living cells. The effect of 6h on the concentration of IFN- gamma in peripheral blood is significant, and the specific mechanism needs further study. According to the previous study, the apoptotic cells have a definite effect on the body and can cause immune tolerance, and the preliminary study of the group was traced by the apoptotic cells, and the apoptotic splenic lymphocytes were found. It mainly aggregates and resides in the liver and has an effect on the microenvironment of cytokine in liver tissue, including the specific secretion level of IL-1 beta, IL-4, IL-10, and IFN- gamma, thus speculates that the apoptotic cells mainly play a role in the liver and have no obvious influence on the outside. Changes in type and response function, such as memory T cells, B cells, etc.
【學(xué)位授予單位】：南方醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2009
【分類號(hào)】：R392

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