本文關鍵詞：腸免疫系統(tǒng)和HIV感染相關免疫學的研究　出處：《暨南大學》2006年碩士論文　論文類型：學位論文

  更多相關文章： 腸道免疫系統(tǒng) 生理性活化 生理性低反應 趨化因子受體 整合素 HIV病 活化 凋亡

【摘要】：本研究旨在探討腸免疫系統(tǒng)有別于系統(tǒng)免疫系統(tǒng)的特征，在此基礎上探討腸相關淋巴組織中淋巴細胞對HIV感染的容許性和HIV復制的支持性，最后，探討AT-2滅活HIV病毒顆粒在HIV感染時所引起的免疫過度活化的分子基礎，為艾滋病以腸道為靶向的新治療策略的制定奠定免疫學基礎。也就是說，通過此研究初步驗證我們所提出的“HIV感染腸道免疫系統(tǒng)過度活化論”工作假說。我們的假說認為：在正常情況下，腸道免疫系統(tǒng)處于生理性活化狀態(tài)和生理性低反應性狀態(tài)，其生理性活化狀態(tài)為HIV感染提供了大量的易感細胞。而在HIV感染時，由于危險信號的釋放，病毒子模擬APc的作用，調節(jié)性T細胞優(yōu)先被刪除等原因導致生理性低反應性狀態(tài)被打破，而出現(xiàn)免疫過度活化，從而產生更多的HIV易感細胞，通過直接感染以及活化誘導細胞凋亡，使腸道T細胞在短期內大量丟失，，從而導致免疫缺陷。為此，我們進行了三個方面的研究：小鼠腸粘膜免疫系統(tǒng)特點分析；人腸道HIV感染容許性和HIV復制支持性分析；HIV感染免疫過度活化機理體外實驗分析。 論文的第一部分，通過對小鼠派氏集合淋巴結(PPs)、腸系膜淋巴結(MLNs)和腹股溝淋巴結(ILNs)的比較性研究，以分析小鼠腸道免疫系統(tǒng)的特點。以往的研究表明，由于腸道是機體營養(yǎng)吸收和共生菌繁殖的主要場所，精確區(qū)分入侵病原微生物和無害的食物和共生菌抗原成為腸粘膜免疫系統(tǒng)的結構和功能進化的原動力。在功能上，腸道免疫系統(tǒng)能十分清楚地區(qū)分哪些是有害的抗原(例如入侵微生物)，哪些是無害的抗原(例如食物抗原和腸道共生菌)，以便作出合適的免疫應答，以清除有害的抗原而對無害的抗原形成耐受，以保護機體免受病理性損傷；在結構上，分為免疫應答“誘導”部位(“inductive”sites)和免疫應答“效應者”部位(“effector”sites)，前者與免疫應答的啟動和免疫耐受的誘導有關，后者參與實施免疫應答的效應者機制。本部分我們采取了以下的研究方法：無菌分離小鼠PPs、
[Abstract]:The purpose of this study is to investigate the intestinal immune system has characteristic different from the immune system, on the basis of lymphocytes of gut associated lymphoid tissue to allow and support HIV replication, HIV infection, finally, to explore the molecular basis of AT-2 inactivated HIV virus particles in the disease caused by HIV infection without excessive activation, for to lay the basic immunology AIDS intestinal develop new therapeutic strategies to target. That is to say, through this study preliminary verification of HIV infection of intestinal immune system we proposed "excessive activation of working hypothesis. Our hypothesis is that: under normal circumstances, the intestinal immune system is in the state of physiological activation and physiological low the reaction of the state, the state of physiological activation provides a large number of susceptible cells for HIV infection. In HIV infection, due to the release of danger signals, adenovirus mimic the role of APc, adjusted T Causes of cell priority is deleted as a result of physiological reactivity is broken, and the emergence of immune activation, resulting in more HIV susceptible cells by direct infection and activation induced cell apoptosis, the intestinal T cell loss in the short term, which leads to immune deficiency. Therefore, we conducted a study of three the analysis of the characteristics of intestinal mucosal immune system in mice; human intestinal HIV infection and the supportiveness of HIV replication of HIV infection; immune activation mechanism analysis in vitro.
The first part of the thesis, through the collection of inflammatory bowel disease lymph node (PPs), mesenteric lymph node (MLNs) and inguinal lymph node (ILNs) of the comparative study, to analysis the characteristics of intestinal immune system in mice. Previous studies showed that, due to intestinal absorption of nutrients is the main place of symbiotic bacteria breeding body, accurate to distinguish the invasion of pathogenic microorganisms and harmless commensal bacteria become food and antigen motive power structure and function of intestinal mucosal immune system evolution. In function, the intestinal immune system can clearly distinguish what is harmful antigens (e.g., which is invading microbes) harmless antigens (e.g. food antigens and commensal bacteria) and in order to make the appropriate immune response, to remove harmful antigen and harmless to antigen tolerance, to protect the body from injury; in the structure, divided into "induced" (part of the immune response" Inductive "sites") and the immune response effect "site (" effector "sites), and the former was related to the induction of immune response priming and immune tolerance, which is involved in the implementation of the effect of the immune response mechanism. In this part, we adopt the following methods: sterile from mouse PPs,

【學位授予單位】：暨南大學
【學位級別】：碩士
【學位授予年份】：2006
【分類號】：R392

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