Differences in antigen-specific CD4+ responses to opportunistic infections in HIV infection
Differences in antigen-specific CD4+ responses to opportunistic infections in HIV infection
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DOI：
10.1002/iid3.50
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发表时间：
2015-09-01
影响因子：
3.2
通讯作者：
Lalvani, Ajit
中科院分区：
文献类型：
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作者：
Pollock, Katrina M.;Montamat-Sicotte, Damien J.;Lalvani, Ajit
严重免疫缺陷的艾滋病毒感染者有机会性感染(OI)的风险。结核病(TB)可能在没有实质性免疫抑制的情况下发生，这表明艾滋病毒对结核分枝杆菌(MTB)特异性细胞介导免疫(CMI)具有早期和持续的不利影响。这项前瞻性观察队列研究旨在观察OI特异性和结核分枝杆菌特异性CMI的差异，这可能是这一点的基础。应用多色流式细胞术，比较了HIV感染者和非HIV感染者对MTB、巨细胞病毒(CMV)、EB病毒(EBV)和白色念珠菌的CD4+反应。MTB特异性的CD4+T细胞比病毒特异性(CMV/EBV)的CD4+T细胞更具多功能，后者主要只分泌干扰素-γ(IFN-γ)。在HIV感染者中，干扰素-α和白介素2(IL-2)双重MTB特异性细胞的频率降低，而在其他病原体中则不明显。MTB特异性细胞分化程度较低，尤其是与CMV特异性细胞相比。在HIV合并感染中，CD127在结核分枝杆菌特异性细胞上的表达相对较少。与EBV特异性的CD4+T细胞相比，MTB特异性的CD4+T细胞PD-1的表达很少。这些CD4+T细胞反应的内在质量的变化和艾滋病毒合并感染的影响可能有助于艾滋病毒感染中合并传染病的发生时间。
HIV-infected individuals with severe immunodeficiency are at risk of opportunistic infection (OI). Tuberculosis (TB) may occur without substantial immune suppression suggesting an early and sustained adverse impact of HIV on Mycobacterium tuberculosis (MTB)-specific cell mediated immunity (CMI). This prospective observational cohort study aimed to observe differences in OI-specific and MTB-specific CMI that might underlie this. Using polychromatic flow cytometry, we compared CD4+ responses to MTB, cytomegalovirus (CMV), Epstein-Barr virus (EBV) and Candida albicans in individuals with and without HIV infection. MTB-specific CD4+ T-cells were more polyfunctional than virus specific (CMV/EBV) CD4+ T-cells which predominantly secreted IFN-gamma (IFN-gamma) only. There was a reduced frequency of IFN-theta and IL-2 (IL-2)-dual-MTBspecificcells in HIV-infected individuals, which was not apparent for the other pathogens. MTB- specific cells were less differentiated especially compared with CMV-specific cells. CD127 expression was relatively less frequent on MTB- specific cells in HIV co-infection. MTB- specific CD4+ T-cells PD-1 expression was infrequent in contrast to EBV-specific CD4+ T-cells. The variation in the inherent quality of these CD4+ T-cell responses and impact of HIV co-infection may contribute to the timing of co-infectious diseases in HIV infection.