骨髓間充質(zhì)干細(xì)胞的免疫調(diào)節(jié)作用及其對(duì)GVHD影響的機(jī)制探討
發(fā)布時(shí)間:2018-06-04 13:43
本文選題:骨髓間充質(zhì)干細(xì)胞 + T淋巴細(xì)胞。 參考:《四川大學(xué)》2006年博士論文
【摘要】:目的 移植物抗宿主病(graft-versus-host disease,,GVHD)是異基因造血干細(xì)胞移植的主要并發(fā)癥。供者T淋巴細(xì)胞識(shí)別宿主抗原提呈細(xì)胞攜帶異基因抗原片斷,進(jìn)一步活化并且分泌大量細(xì)胞因子,從而造成宿主的組織損傷。雖然許多標(biāo)準(zhǔn)的GVHD預(yù)防方案已經(jīng)廣泛應(yīng)用于異基因造血干細(xì)胞移植術(shù)后,但重度的GVHD,尤其是激素難治型GVHD仍然嚴(yán)重威脅患者的生命。 aGVHD發(fā)生中的效應(yīng)階段包括體液免疫和細(xì)胞免疫兩方面,即活化的T淋巴細(xì)胞釋放大量的炎癥因子,如TNF-α、IL-1等,同時(shí)自然殺傷細(xì)胞和細(xì)胞毒性淋巴細(xì)胞產(chǎn)生的細(xì)胞毒作用,兩者共同作用造成了宿主的組織損傷。Ⅰ型T淋巴細(xì)胞分泌細(xì)胞因子如IL-2,IFNγ,這些炎癥因子促使單核巨噬細(xì)胞活化,對(duì)炎癥的形成起重要的作用,這些作用可以被Ⅱ型T細(xì)胞所分泌的免疫負(fù)調(diào)節(jié)細(xì)胞因子IL-4和IL-10所抑制。aGVHD的發(fā)生主要是以Ⅰ型T淋巴細(xì)胞產(chǎn)生的強(qiáng)烈的免疫反應(yīng),減少Ⅰ型T細(xì)胞的產(chǎn)生,增加Ⅱ型T細(xì)胞的比例,可以減低GVHD所導(dǎo)致的移植相關(guān)死亡率;罨腡淋巴細(xì)胞的遷移在GVHD發(fā)病機(jī)制中起了至
[Abstract]:Purpose Graft-versus-host disease (GVHD) is a major complication of allogeneic hematopoietic stem cell transplantation (HSCT). Donor T lymphocytes recognize host antigen-presenting cells carrying allogeneic antigen fragments and further activate and secrete a large number of cytokines resulting in host tissue damage. Although many standard prophylaxis of GVHD have been widely used after allogeneic hematopoietic stem cell transplantation, severe GVHD, especially steroid refractory GVHD, still pose a serious threat to the life of patients. The effect stages of aGVHD include humoral immunity and cellular immunity. The activated T lymphocytes release a large number of inflammatory factors, such as TNF- 偽, IL-1, and the cytotoxic effects of natural killer cells and cytotoxic lymphocytes. The cytokines secreted by T lymphocytes of type 鈪
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