Saharia Kapil K, Petrovas Constantinos, Ferrando-Martinez Sara, Leal Manuel, Luque Rafael, Ive Prudence, Luetkemeyer Anne, Havlir Diane, Koup Richard A
Institute of Human Virology and Division of Infectious Diseases, University of Maryland School of Medicine, Baltimore, MD, United States of America.
Immunology Laboratory, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, United States of America.
PLoS One. 2016 Jul 1;11(7):e0158262. doi: 10.1371/journal.pone.0158262. eCollection 2016.
Little is known about the expression of inhibitory molecules cytotoxic T-lymphocyte antigen-4 (CTLA-4) and programmed-death-1 (PD-1) on Mycobacterium tuberculosis (Mtb)-specific CD4 T-cells and how their expression is impacted by TB treatment.
Cryopreserved PBMCs from HIV-TB co-infected and TB mono-infected patients with untreated and treated tuberculosis (TB) disease were stimulated for six hours with PPD and stained. Using polychromatic flow cytometry, we characterized the differentiation state, cytokine profile, and inhibitory molecule expression on PPD-specific CD4 T-cells.
In our HIV-TB co-infected cohort, TB treatment increased the proportion of PPD-specific CD4 T-cells co-producing IFN-γ+IL-2+TNF-α+ and IFN-γ+IL-2+ (p = 0.0004 and p = 0.0002, respectively) while decreasing the proportion of PPD-specific CD4 T-cells co-producing IFN-γ+MIP1-β+TNF-α+ and IFN-γ+MIP1-β+. The proportion of PPD-specific CD4 T-cells expressing an effector memory phenotype decreased (63.6% vs 51.6%, p = 0.0015) while the proportion expressing a central memory phenotype increased (7.8% vs. 21.7%, p = 0.001) following TB treatment. TB treatment reduced the proportion of PPD-specific CD4 T-cells expressing CTLA-4 (72.4% vs. 44.3%, p = 0.0005) and PD-1 (34.5% vs. 29.2%, p = 0.03). Similar trends were noted in our TB mono-infected cohort.
TB treatment alters the functional profile of Mtb-specific CD4 T-cells reflecting shifts towards a less differentiated maturational profile and decreases PD-1 and CTLA-4 expression. These could serve as markers of reduced mycobacterial burden. Further study is warranted.
关于结核分枝杆菌(Mtb)特异性CD4 T细胞上抑制性分子细胞毒性T淋巴细胞抗原4(CTLA-4)和程序性死亡1(PD-1)的表达以及它们的表达如何受到结核病治疗的影响,人们了解甚少。
用PPD刺激来自HIV-TB合并感染和单纯TB感染患者的未经治疗和经治疗的结核病患者的冻存外周血单核细胞(PBMC)6小时,然后进行染色。使用多色流式细胞术,我们对PPD特异性CD4 T细胞的分化状态、细胞因子谱和抑制性分子表达进行了表征。
在我们的HIV-TB合并感染队列中,结核病治疗增加了共同产生IFN-γ+IL-2+TNF-α+和IFN-γ+IL-2+的PPD特异性CD4 T细胞的比例(分别为p = 0.0004和p = 0.0002),同时降低了共同产生IFN-γ+MIP1-β+TNF-α+和IFN-γ+MIP1-β+的PPD特异性CD4 T细胞的比例。结核病治疗后,表达效应记忆表型的PPD特异性CD4 T细胞比例降低(63.6%对51.6%,p = 0.0015),而表达中央记忆表型的比例增加(7.8%对21.7%,p = 0.001)。结核病治疗降低了表达CTLA-4的PPD特异性CD4 T细胞的比例(72.4%对44.3%,p = 0.0005)和PD-1的比例(34.5%对29.2%,p = 0.03)。在我们的单纯TB感染队列中也观察到了类似趋势。
结核病治疗改变了Mtb特异性CD4 T细胞的功能谱,反映出向分化程度较低的成熟谱转变,并降低了PD-1和CTLA-4的表达。这些可作为分枝杆菌负荷降低的标志物。有必要进行进一步研究。