摘要
脓毒症可同时存在免疫功能亢进和抑制，在此过程中，T淋巴细胞凋亡发挥重要作用，其所导致的免疫细胞数量，功能的变化，是导致脓毒症患者从免疫功能亢进到抑制乃至麻痹的一个重要因素。在T淋巴细胞的凋亡过程中，Treg、DC、TNF—α及其受体、Bcl家族、IL-2等起着重要的调节作用，这些物质相互作川，最终造成了T细胞凋亡，引起免疫抑制，使病原体难以清除，且易于继发感染。针对与T淋巴细胞凋亡有关的因素进行治疗有了长足进步，并在一定程度上抑制了T细胞凋亡，但却未能达到应有的效果，也未能改善患者的预后，究其原因多在于对脓毒症机制的认识有一定局限性，为了进一步阐明脓毒症的发生机理。
During sepsis, the immune hyperfunetion and suppression can coexist. T lymphocyte apoptosis plays an important role in immune dysfunction. The quantitative and functional alterations of T lymphocytes make immune hyperfunction drifting to suppression or even paralysis. In this process, Treg, DC, TNF-α and its receptor, Bcl family, interleukin-2 and other cytokines play important roles. The interactions of these substances ultimately result in the apoptosis of T-cells, and immune suppression, which in turn leads to difficulty to removed the pathogens and secondary infection. It was found that the treatment aimed at the regulative factors of T lymphocyte apoptosis can inhibit T lymphocyte apoptosis to some extent. However, an effective way to suppress T- cell apoptosis has not been found, and the prognosis of patients was not improved in the applicaion of this approach. The reasons might lie on the limited understanding of the mechanism of the occurrence and development of sepsis.
出处
《国际免疫学杂志》
CAS
北大核心
2009年第6期483-487,共5页
International Journal of Immunology
基金
国家自然基金资助项目（30872378,J0730860）
