Особенности потребления глюкозы субпопуляциями CD4 + Т-лимфоцитов у ВИЧ-инфицированных пациентов, получающих антиретровирусную терапию

Metabolism of glucose, a universal biosynthetic substrate in CD4 + T lymphocytes, is increased in HIV-infection. However, the issue of heterogeneity in glucose consumption by the CD4 + T cell subsets remains unresolved. The aim of this work was to assess glucose uptake by resting and cycling naive and memory CD4 + T cells in HIV-infected patients receiving antiretroviral therapy. We examined 47 subjects, 26 of whom were infected with HIV and were administered antiretroviral drugs. The following indices were determined: the number of CD4 + T lymphocytes, size of naive (CD4 + CD45R0-) and memory (CD4 + CD45R0 + ) T cell subsets, frequencies of resting (CD71 - ) and cycling (CD71 + ) cell forms in each subset, the glucose fluorescent analog (2-NBDG) uptake by various CD4 + T cell subsets. It was shown that, regardless of HIV status, the CD4+T cells are active glucose consumers. Cycling lymphocytes, compared with resting cells, uptake more biosynthetic substrate. We have revealed a trend for increased glucose uptake in HIV-infected patients when compared with healthy individuals. Memory cells, in comparison with naive lymphocytes, consume the substrate more actively, independent on HIV status. At the same time, naive CD4 + T lymphocytes of HIV-infected individuals capture more glucose than the corresponding cell subset in non-infected donors. Cycling naive CD4 + T lymphocytes of HIV-positive subjects are more active consumers of glucose than the analogues in healthy subjects. No differences were found between HIV-positive and HIV-negative groups for intensity of substrate consumption by the cycling memory CD4 + T cells. Thus, in treated HIV-infected patients, CD4 + T cells seem to uptake more glucose than similar cell subpopulations in healthy people, which, apparently, is mediated by the activity of resting naive lymphocytes. The data obtained indicate that metabolic characteristics in resting T-cells are instable and may change depending on the substrate availability.