本文關(guān)鍵詞：C5aR基因缺失小鼠對(duì)局部L.major感染的抵抗作用　出處：《南華大學(xué)》2012年碩士論文　論文類型：學(xué)位論文

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【摘要】：目的：研究C5a/C5aR通路對(duì)BALB/c小鼠局部L.major感染敏感性的影響及對(duì)CD4+T細(xì)胞免疫應(yīng)答的調(diào)節(jié)作用。 方法：經(jīng)皮下注射對(duì)各受試組小鼠腳掌進(jìn)行感染；利用電子卡尺每周定時(shí)監(jiān)測(cè)受感染腳掌與未感染腳掌病損厚度之差，觀察比較野生型BALB/c和C5aR基因缺失小鼠在不同劑量L.major感染后的病損變化；利用有限稀釋法檢測(cè)了各組感染小鼠體內(nèi)寄生蟲(chóng)的負(fù)荷；在常規(guī)劑量（1×10~6/mouse）L.major感染條件下，，使用ELISA法檢測(cè)受試小鼠受引流淋巴結(jié)細(xì)胞體外重刺激培養(yǎng)上清中CD4+Th1相關(guān)細(xì)胞因子IFN-γ的濃度，并進(jìn)一步通過(guò)ELISA和FACS檢測(cè)了CD4+Th1及Th2相關(guān)細(xì)胞因子IL-17和IL-4的產(chǎn)生。 結(jié)果：在常規(guī)劑量(1×10~6/mouse) L.major感染條件下，C5aR基因缺失小鼠感染L.major后的病損程度與感染部位寄生蟲(chóng)負(fù)荷均顯著低于野生型BALB/c小鼠，但在高劑量(5×10~6/mouse)感染條件下，上述指標(biāo)在兩組小鼠間無(wú)明顯差異；ELISA結(jié)果顯示細(xì)胞因子IFN-γ的產(chǎn)生在感染后的C5aR基因缺失與野生型小鼠間無(wú)顯著差異；FACS胞內(nèi)染色結(jié)果表明感染后的C5aRKO小鼠CD4+IL-4+T細(xì)胞亞群百分比顯著低于野生型BALB/c小鼠感染組，但CD3+IL-17+T細(xì)胞亞群的百分比在兩組之間無(wú)顯著差異。 結(jié)論：1. C5a/C5aR信號(hào)通路在常規(guī)劑量(1×10~6/mouse) L.major感染條件下，可介導(dǎo)野生型BALB/c小鼠對(duì)L.major的敏感性，而缺失C5aR基因阻斷這一通路有助于降低感染程度；但當(dāng)L.major劑量達(dá)到5×10~6/mouse時(shí)，C5aR基因缺失與否對(duì)感染程度沒(méi)有影響。 2. C5a/C5aR信號(hào)通路在L.major感染的BALB/c小鼠中可能主要通過(guò)調(diào)節(jié)Th2細(xì)胞因子IL-4的產(chǎn)生，進(jìn)而誘導(dǎo)Th2免疫應(yīng)答的分化，加劇易感小鼠的L.major受感染部位的病損程度。
[Abstract]:Objective : To study the effect of C5a / C5a1pathway on the sensitivity of local L . major infection in BALB / c mice and its effect on the immune response of CD4 + T cells . Methods : The levels of CD4 + Th1 - related cytokines IL - 17 and IL - 4 were detected by ELISA and FACS . The levels of CD4 + Th1 - related cytokines IFN - 緯 were detected by ELISA and FACS . Results : Under the condition of normal dose ( 1 脳 10 ~ 6 / mouse ) L . major infection , there was no significant difference between the severity of the disease and the parasitic load of the infected site . The results showed that the percentage of CD4 + IL - 4 + T cells in the infected C5aRKO mice was significantly lower than that of wild - type BALB / c mice . The results showed that the percentage of CD4 + IL - 4 + T cells in the infected C5aRKO mice was significantly lower than that of wild type BALB / c mice . Conclusion : 1 . The C5a / C5a1signal pathway can mediate the susceptibility of wild - type BALB / c mice to L . major in the normal dose ( 1 脳 10 ~ 6 / mouse ) L . Major infection conditions , while the deletion of C5a1gene blocks this pathway to reduce the degree of infection . However , when the major dose of L . major reaches 5 脳 10 ~ 6 / mouse , the deletion of C5a1gene has no effect on the degree of infection . 2 . In BALB / c mice infected with L . major infection , C5a / C5a1signal pathway may mainly regulate the production of Th2 cytokine IL - 4 , thus inducing differentiation of Th2 immune response and increasing the degree of disease damage in L . major infected part of susceptible mice .

【學(xué)位授予單位】：南華大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R392

【參考文獻(xiàn)】

相關(guān)期刊論文 前1條

1 尚宇航;姜曼;楊菲;曹朝暉;董世訪;江偉凡;陳戩;吳玉章;許桂蓮;;LIHGT-HVEM/LTbR途徑缺陷誘導(dǎo)T細(xì)胞的失能[J];免疫學(xué)雜志;2010年09期

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