Obeagu Emmanuel Ifeanyi, Iyengar Raajasiri
Department of Biomedical and Laboratory Science, Africa University, Zimbabwe.
Department of GA, India.
Ann Med Surg (Lond). 2025 Jul 22;87(9):5807-5813. doi: 10.1097/MS9.0000000000003631. eCollection 2025 Sep.
Regulatory T cells (Tregs) are pivotal in maintaining immune homeostasis by suppressing excessive immune responses, thereby preventing immunopathology. In the context of infant human immunodeficiency virus (HIV) infection, Tregs exhibit a dualistic role: while they mitigate immune activation, they may also impede effective antiviral immunity, facilitating viral persistence. Recent studies have illuminated the nuanced involvement of Tregs in infant HIV pathogenesis. For instance, research has demonstrated that HIV-exposed uninfected infants exhibit lower frequencies of peripheral blood Tregs at birth compared to unexposed infants, leading to a delayed expansion of these cells over the first 36 weeks of life. This disruption in Treg development is associated with gut epithelial damage, suggesting that compromised mucosal integrity may influence Treg dynamics in early life. Tregs influence HIV pathogenesis in infants through several mechanisms. They suppress the activation and proliferation of effector T cells, including HIV-specific CD8+ cytotoxic T lymphocytes, which are crucial for controlling viral replication. This suppression can lead to inadequate immune responses against HIV, allowing the virus to persist and replicate. Additionally, Tregs can modulate the function of dendritic cells, leading to suboptimal antigen presentation and further dampening the adaptive immune response. Moreover, an imbalance between Tregs and Th17 cells, another subset of CD4+ T cells involved in mucosal immunity, has been observed in HIV-infected individuals. The loss of Th17 cells, coupled with an increase in Tregs, can compromise mucosal barriers, facilitating microbial translocation and chronic immune activation, which are hallmarks of HIV disease progression.
调节性T细胞（Tregs）在通过抑制过度免疫反应来维持免疫稳态方面起着关键作用，从而预防免疫病理。在婴儿人类免疫缺陷病毒（HIV）感染的背景下，Tregs发挥着双重作用：虽然它们减轻免疫激活，但也可能阻碍有效的抗病毒免疫，促进病毒持续存在。最近的研究阐明了Tregs在婴儿HIV发病机制中的细微作用。例如，研究表明，与未接触HIV的婴儿相比，接触过HIV但未感染的婴儿出生时外周血Tregs频率较低，导致这些细胞在生命的前36周内扩张延迟。Treg发育的这种破坏与肠道上皮损伤有关，这表明受损的粘膜完整性可能影响生命早期的Treg动态。Tregs通过多种机制影响婴儿的HIV发病机制。它们抑制效应T细胞的激活和增殖，包括对控制病毒复制至关重要的HIV特异性CD8+细胞毒性T淋巴细胞。这种抑制可导致对HIV的免疫反应不足，使病毒得以持续存在和复制。此外，Tregs可调节树突状细胞的功能，导致抗原呈递不佳，并进一步抑制适应性免疫反应。此外，在HIV感染者中观察到Tregs与Th17细胞（参与粘膜免疫的另一种CD4+T细胞亚群）之间的失衡。Th17细胞的丧失，加上Tregs的增加，会损害粘膜屏障，促进微生物易位和慢性免疫激活，这是HIV疾病进展的标志。
