Department of Immunology and Molecular Biology, Makerere University College of Health Sciences, P. O. Box 7072, Kampala, Uganda.
MRC/UVRI Uganda Research Unit on AIDS and London School of Hygiene & Tropical Medicine, London, UK.
AIDS Res Ther. 2018 Mar 15;15(1):7. doi: 10.1186/s12981-018-0194-y.
HIV infection causes upregulation of markers of inflammation, immune activation and apoptosis of host adaptive, and innate immune cells particularly monocytes, natural killer (NK) and innate lymphoid cells (ILCs). Although antiretroviral therapy (ART) restores CD4 T-cell counts, the persistent aberrant activation of monocytes, NK and ILCs observed likely contributes to the incomplete recovery of T-cell effector functions. A better understanding of the effects of HIV infection and ART on the phenotype and function of circulating monocytes, NK, and ILCs is required to guide development of novel therapeutic interventions to optimize immune recovery.
HIV 感染导致宿主适应性和先天免疫细胞（尤其是单核细胞、自然杀伤细胞（NK）和固有淋巴细胞（ILC））的炎症标志物、免疫激活和凋亡上调。尽管抗逆转录病毒疗法（ART）可恢复 CD4 T 细胞计数，但观察到的单核细胞、NK 和 ILC 持续异常激活可能导致 T 细胞效应功能不完全恢复。需要更好地了解 HIV 感染和 ART 对循环单核细胞、NK 和 ILC 表型和功能的影响，以指导开发新的治疗干预措施来优化免疫恢复。
