Background Chronic inflammation is prevalent with ART-suppressed HIV-infection and one immune cell subset putatively driving this phenomenon is TIGIT + γδ T cells Methods To elucidate γδ T cell phenotypic diversity, spectral flow cytometry was performed on blood lymphocytes from individuals of an HIV and Aging cohort and data were analyzed using bioinformatic platforms. Plasma inflammatory markers were measured and correlated with γδ T cell subset frequencies. Results 39 distinct γδ T cell subsets were identified (22 Vδ1+, 14 Vδ2+, and three Vδ1-Vδ2-Vγ9+) and TIGIT was nearly exclusively found on the Vδ1+ CD45RA+ CD27- ‘effector’ populations. People living with ART-suppressed HIV-infection (PLWH) exhibited high frequencies of distinct clusters of Vδ1+ effectors distinguished via CD8, CD56, CD16, and CD38 expression. Among Vδ2+ cells, most Vγ9+ (‘innate-effector’) clusters were lower in PLWH, yet CD27+ subsets were similar in frequency between participants with and without HIV. Comparisons by age revealed lower ‘naïve’ Vδ1 + CD45RA+ CD27+ in older individuals, regardless of HIV status. Plasma inflammatory markers were selectively linked to subsets of Vδ1+ and Vδ2+ cells. Conclusions These results further elucidate γδ T cell subset complexity and reveal distinct alterations and connections with inflammatory pathways of Vδ1+ effector and Vδ2+ innate-effector subsets with ART-suppressed HIV infection.

中文翻译：

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在 ART 抑制的 HIV 感染期间，Vδ1 效应细胞和 Vδ2 γδ T 细胞的不同亚群频率发生变化，并与血浆炎症标志物相关

背景 慢性炎症在 ART 抑制的 HIV 感染中普遍存在，推定驱动这一现象的一个免疫细胞亚群是 TIGIT + γδ T 细胞 方法 为了阐明 γδ T 细胞表型多样性，对 HIV 个体的血液淋巴细胞进行了光谱流式细胞术使用生物信息平台分析老龄化队列和数据。测量血浆炎症标志物并与 γδ T 细胞亚群频率相关。结果 鉴定出 39 个不同的 γδ T 细胞亚群（22 个 Vδ1+、14 个 Vδ2+ 和 3 个 Vδ1-Vδ2-Vγ9+），TIGIT 几乎只在 Vδ1+ CD45RA+ CD27-“效应细胞”群体中发现。ART 抑制的 HIV 感染 (PLWH) 患者表现出高频率的不同 Vδ1+ 效应器簇，通过 CD8、CD56、CD16 和 CD38 表达进行区分。在 Vδ2+ 细胞中，大多数 Vγ9+（“先天效应细胞”）簇在 PLWH 中较低，但 CD27+ 亚群在感染和未感染 HIV 的参与者之间的频率相似。按年龄进行比较显示，无论 HIV 状况如何，老年人的“初始”Vδ1 + CD45RA+ CD27+ 较低。血浆炎症标记物选择性地与 Vδ1+ 和 Vδ2+ 细胞亚群相关。结论 这些结果进一步阐明了 γδ T 细胞亚群的复杂性，并揭示了 ART 抑制的 HIV 感染中 Vδ1+ 效应子和 Vδ2+ 先天效应子亚群的炎症途径的明显改变和联系。