NLRP3炎症小体在HIV/AIDS中的作用与分子机制研究进展

Research progress in role and molecular mechanismsof NLRP3 inflammasome in HIV/AIDS

  • 摘要: CD4+T细胞耗竭是人类免疫缺陷病毒(HIV)感染的标志性病理特征,也是导致获得性免疫缺陷综合征(AIDS)发生的关键因素,但其耗竭背后的机制仍未完全阐明。同时,联合抗逆转录病毒治疗虽能有效抑制HIV病毒复制,减轻免疫功能损伤并降低病死率,但其无法根除体内病毒库,并且长期用药存在机体耐药性和药物不良反应等问题。因此,开发新型HIV/AIDS治疗策略依然十分迫切。NOD样受体热蛋白结构域相关蛋白3(NLRP3炎症小体)在CD4+T细胞耗竭及HIV/AIDS病程中发挥着重要调控作用,对其进行精准干预有望成为新的治疗靶点。基于此,本文系统梳理了NLRP3炎症小体在HIV/AIDS不同阶段的激活机制和功能效应,旨在为识别潜在治疗靶点和拓展 HIV/AIDS干预策略提供理论依据。

     

    Abstract: The depletion of CD4+T cells is a hallmark pathological feature of Human Immunodeficiency Virus (HIV) infection and a key factor contributing to the development of Acquired Immune Deficiency Syndrome (AIDS). However, the mechanisms underlying this depletion remain incompletely elucidated. Meanwhile, although combined Antiretroviral Therapy (cART) can effectively suppress HIV replication, alleviate immune dysfunction and reduce mortality, it fails to eradicate the viral reservoir in the body. Furthermore, long-term medication is associated with issues such as drug resistance and adverse reactions. Consequently, the development of novel therapeutic strategies for HIV/AIDS remains an urgent priority. NOD-like receptor thermal protein domain-associated protein 3 (NLRP3 inflammasome) plays a crucial regulatory role in the depletion of CD4+T cells and the progression of HIV/AIDS, and precise intervention targeting it holds promise as a new therapeutic target. This study systematically summarizes the activation mechanisms and functional effects of the NLRP3 inflammasome at different stages of HIV/AIDS, aiming to provide a theoretical basis for identifying potential therapeutic targets and expanding intervention strategies for HIV/AIDS.

     

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