Kestens Luc, Seddiki Nabila, Bohjanen Paul R
Immunology Unit, Department of Microbiology, Institute of Tropical Medicine, B-2000 Antwerpen, Belgium.
Curr Opin HIV AIDS. 2008 Jul;3(4):419-24. doi: 10.1097/COH.0b013e328302ebbb.
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.
本文旨在回顾关于病原体相关免疫重建疾病免疫发病机制的最新文献，并讨论免疫激活以及巨噬细胞、效应和调节性T细胞、自然杀伤细胞等各种效应分子和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HIV患者会发生免疫重建疾病，其特征是对正在复制或已死亡的病原体产生过度的炎症免疫反应。在大多数此类病例中，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反应的恢复有关。引发免疫重建疾病的确切条件尚未确定。免疫重建疾病患者存在明显的免疫激活，这可能是由于接受抗逆转录病毒治疗的患者在最初免疫快速恢复后体内稳态控制不佳所致。免疫重建疾病患者体内稳态控制不佳可能与效应T细胞和调节性T细胞的恢复失衡有关。
尽管免疫重建疾病的确切机制尚不清楚，但它可能与病原体特异性免疫反应的快速恢复以及体内稳态控制不佳有关，后者会促进过度的免疫病理反应，尤其是在存在高浓度活病原体或病原体碎片的情况下。
