Glucose uptake by CD4+Т cell subsets in HIV-infected patients receiving highly active antiretroviral therapy (haart)

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Abstract

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.

About the authors

L. B. Korolevskaya

Institute of Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm Federal Research Center, Ural Branch, Russian Academy of Sciences

Author for correspondence.
Email: bioqueen@mail.ru

Larisa B. Korolevskaya - PhD (Medicine), Research Associate, Laboratory of Ecological Immunology, Institute of Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm Federal Research Center, Ural Branch, Russian Academy of Sciences.

614081, Perm, Golev str., 13.

Phone: 7 (342) 280-83-34.

Fax: 7 (342) 280-92-11.

Russian Federation

E. V. Saidakova

Institute of Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm Federal Research Center, Ural Branch, Russian Academy of Sciences

Email: radimira@list.ru

PhD (Biology), Senior Research Associate, Laboratory of Ecological Immunology, Institute of Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm Federal Research Center, Ural Branch, Russian Academy of Sciences.

614081, Perm, Golev str., 13.

Russian Federation

V. V. Vlasova

Institute of Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm Federal Research Center, Ural Branch, Russian Academy of Sciences

Email: violetbaudelaire73@gmail.com

Laboratory Assistant, Laboratory of Ecological Immunology, Institute of Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm Federal Research Center, Ural Branch, Russian Academy of Sciences.

614081, Perm, Golev str., 13.

Russian Federation

K. V. Shmagel

Institute of Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm Federal Research Center, Ural Branch, Russian Academy of Sciences

Email: shmagel@iegm.ru

PhD, MD (Medicine), Head, Laboratory of Ecological Immunology, Institute of Ecology and Genetics of Microorganisms, Ural Branch, Russian Academy of Sciences, Perm Federal Research Center, Ural Branch, Russian Academy of Sciences.

614081, Perm, Golev str., 13.

Russian Federation

References

  1. Fry T.J., Connick E., Falloon J., Lederman M.M., Liewehr D.J., Spritzler J. A potential role for interleukin-7 in T-cell homeostasis. Blood, 2001, Vol. 97, no. 10, pp. 2983-2990.
  2. Jones R.G., Thompson C.B. Revving the engine: signal transduction fuels T cell activation. Immunity, 2007, Vol. 27, no. 2, pp. 173-178.
  3. Korencak M., Byrne M., Richter E., Schultz B.T., Juszczak P., Ake J.A. Effect of HIV infection and antiretroviral therapy on immune cellular functions. JCI Insight, 2019, Vol. 4, no. 12, e126675. doi: 10.1172/jci.insight.126675.
  4. Masson J.J.R., Murphy A.J., Lee M.K.S., Ostrowski M., Crowe S.M., Palmer C.S. Assessment of metabolic and mitochondrial dynamics in CD4+ and CD8+ T cells in virologically suppressed HIV-positive individuals on combination antiretroviral therapy. PLoS One, 2017, Vol. 12, no. 8, e0183931. doi: 10.1371/journal.pone.0183931.
  5. Napolitano L.A., Grant R.M., Deeks S.G., Schmidt D., de Rosa S.C., Herzenberg L.A. Increased production of IL-7 accompanies HIV-1-mediated T-cell depletion: implications for T-cell homeostasis. Nat. Med., 2001, Vol. 7, no. 1, pp. 73-79.
  6. Sun H., Li X. Metabolic reprogramming in resting and activated immune cells. Metabolomics (Los Angel), 2017, Vol. 7, no. 1, 188. doi: 10.4172/2153-0769.1000188.
  7. Wofford J.A., Wieman H.L., Jacobs S.R., Zhao Y., Rathmell J.C. IL-7 promotes Glut1 trafficking and glucose uptake via STAT5-mediated activation of Akt to support T-cell survival. Blood, 2008, Vol. 111, no. 4, pp. 2101-2111.

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Copyright (c) 2021 Korolevskaya L.B., Saidakova E.V., Vlasova V.V., Shmagel K.V.

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