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感染人类免疫缺陷病毒(HIV)后,引起免疫系统的持续激活,进而导致CD4+T细胞数目不断减少,最终导致人类免疫缺陷综合征(AIDS)的发生。阻断免疫系统的持续激活,可能是减缓AIDS发展进程的重要途径。有研究表明,Toll样受体(TLR)与HIV感染后免疫系统的持续激活密切相关。同时,TLR是重要的模式识别受体,在抗微生物的非特异性免疫中发挥重要作用并参与调节特异性免疫。本文综述了TLR与HIV-1的关系,以给HIV-1治疗及疫苗的研究提供参考。
Infection with human immunodeficiency virus (HIV) causes a sustained activation of the immune system, which in turn leads to a declining number of CD4 + T cells, eventually leading to the development of human immunodeficiency syndrome (AIDS). Blocking the sustained activation of the immune system may be an important way to slow the progression of AIDS. Studies have shown that Toll-like receptors (TLRs) are closely related to the ongoing activation of the immune system after HIV infection. At the same time, TLRs are important pattern recognition receptors that play an important role in antimicrobial nonspecific immunity and are involved in the regulation of specific immunity. This review summarizes the relationship between TLR and HIV-1 to provide a reference for HIV-1 therapy and vaccine research.