Immunopathogenesis of immune reconstitution disease in HIV patients responding to antiretroviral therapy.
Immunopathogenesis of immune reconstitution disease in HIV patients responding to antiretroviral therapy.
复制标题
对抗逆转录病毒疗法反应的HIV患者免疫重建疾病的免疫发病发生。
DOI：
10.1097/coh.0b013e328302ebbb
复制
发表时间：
2008-07
影响因子：
4.1
通讯作者：
Bohjanen PR
中科院分区：
文献类型：
--
作者：
Kestens L;Seddiki N;Bohjanen PR
本文的目的是回顾最新的文献有关病原体相关的免疫重建疾病的免疫发病机制，并讨论免疫激活和各种效应分子和细胞，如巨噬细胞，效应和调节性T细胞，和自然杀伤细胞在免疫重建疾病中的作用。许多接受抗逆转录病毒治疗的艾滋病毒患者发展为免疫重建疾病，其特征是对复制或死亡病原体的过度炎症免疫反应。在大多数情况下，免疫重建疾病与涉及CD4+或CD8+效应T细胞的病原体特异性细胞免疫应答的恢复有关。触发免疫重建疾病的确切条件尚未确定。免疫重建疾病患者具有明显的免疫激活，这可能是由于接受抗逆转录病毒治疗的患者在快速初始免疫恢复后的稳态控制不良。免疫重建疾病患者体内平衡控制不良可能与效应和调节T细胞的不平衡恢复有关。虽然免疫重建疾病的确切机制尚未完全了解，但它可能与病原体特异性免疫应答的快速恢复和促进过度免疫病理学应答的不良稳态控制有关，特别是如果存在高浓度的活病原体或病原体碎片。
The aim of this article is to review the most recent literature regarding the immunopathogenesis of pathogen-associated immune reconstitution disease and to discuss the role of immune activation and various effector molecules and cells such as macrophages, effector and regulatory T cells, and natural killer cells in immune reconstitution disease. Many HIV patients receiving antiretroviral treatment develop immune reconstitution disease, which is characterized by exaggerated inflammatory immune responses to replicating or dead pathogens. In the majority of these cases, immune reconstitution disease is associated with restoration of pathogen-specific cellular immune responses involving CD4+ or CD8+ effector T cells. The precise conditions that trigger immune reconstitution disease have not yet been identified. Immune reconstitution disease patients have overt immune activation, which may be due to poor homeostatic control after the fast initial immune recovery in patients receiving antiretroviral therapy. Poor homeostatic control in immune reconstitution disease patients may be linked to unbalanced restoration of effector and regulatory T cells. Although the precise mechanism of immune reconstitution disease is not well understood, it is probably related to rapid restoration of pathogen-specific immune responses and poor homeostatic control that promote exaggerated immunopathological responses, especially if viable pathogens or pathogen debris are present at high concentrations.