He Sijia, Zhang Zining, Fu Yajing, Qin Chaolong, Li Sha, Han Xiaoxu, Xu Junjie, Liu Jing, Jiang Yongjun, Shang Hong
*Key Laboratory of AIDS Immunology of National Health and Family Planning Commission, Department of Laboratory Medicine, The First Affiliated Hospital, China Medical University, Shenyang, China; †Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, China; and ‡Department of Clinical Laboratory, Dongying People's Hospital, Dongying, China.
J Acquir Immune Defic Syndr. 2015 Dec 15;70(5):472-8. doi: 10.1097/QAI.0000000000000801.
In HIV disease course, the decline of peripheral CD4 T-cell count correlates with rapid disease progression. The supply of peripheral naive T cells by the thymus requires precursor T-cell proliferation within the thymus. In the setting of HIV-1 infection, when both naive and memory T cells are progressively depleted, the contribution of thymic dysfunction in CD4 depletion needs to be studied. Previous research has shown that thymic function may also be impaired in HIV-1 infection. However, it is inconclusive regarding whether this impairment occurred at the early time or during the chronic phase. In addition, the relationship between thymic dysfunction and disease progression remains unknown. In this study, we examined the thymic function in 65 HIV-infected individuals. Among them, 17 were in acute phase, 15 were in early chronic phase, 15 were in chronic phase with no ART (antiretroviral therapy), and 18 were on ART. We also included 11 uninfected individuals as controls. We measured the peripheral blood levels of T-cell receptor rearrangement excision circles and PTK7 and CD31 expressions for the frequency of circulating recent thymic emigrants. We observed that the 2 indicators of thymic function, sj/β-TREC and PTK7, seemed to be lower in the chronic infection group than those in the acute and early chronic groups. Both indicators returned to the normal level after ART. However, after 1-year follow-up of patients with early HIV-1 infection, rapid progressors (n = 4) had lower PTK7 and CD31 expressions than chronic progressors (n = 6).
在HIV疾病进程中，外周血CD4 T细胞计数的下降与疾病的快速进展相关。胸腺对外周血初始T细胞的供应需要胸腺内前体T细胞的增殖。在HIV-1感染的情况下，当初始T细胞和记忆T细胞都逐渐耗竭时，需要研究胸腺功能障碍在CD4细胞耗竭中的作用。先前的研究表明，HIV-1感染时胸腺功能也可能受损。然而，这种损害是发生在早期还是慢性期尚无定论。此外，胸腺功能障碍与疾病进展之间的关系仍然未知。在本研究中，我们检测了65例HIV感染个体的胸腺功能。其中，17例处于急性期，15例处于慢性早期，15例处于未接受抗逆转录病毒治疗（ART）的慢性期，18例正在接受ART治疗。我们还纳入了11例未感染个体作为对照。我们测量了外周血中T细胞受体重排切除环以及PTK7和CD31的表达，以确定循环中近期胸腺迁出细胞的频率。我们观察到，胸腺功能的两个指标，sj/β-TREC和PTK7，在慢性感染组似乎低于急性和慢性早期组。ART治疗后这两个指标均恢复到正常水平。然而，对早期HIV-1感染患者进行1年随访后，快速进展者（n = 4）的PTK7和CD31表达低于慢性进展者（n = 6）。
