Human Immunodeficiency Virus Type-1 Elite Controllers Maintain Low Co-Expression of Inhibitory Receptors on CD4+ T Cells

Front Immunol. 2018 Jan 22:9:19. doi: 10.3389/fimmu.2018.00019. eCollection 2018.

Abstract

Human immunodeficiency virus type-1 (HIV-1) elite controllers (ELCs) represent a unique population that control viral replication in the absence of antiretroviral therapy (cART). It is well established that expression of multiple inhibitory receptors on CD8+ T cells is associated with HIV-1 disease progression. However, whether reduced co-expression of inhibitory receptors on CD4+ T cells is linked to natural viral control and slow HIV-1 disease progression remains undefined. Here, we report on the expression pattern of numerous measurable inhibitory receptors, associated with T cell exhaustion (programmed cell death-1, CTLA-4, and TIGIT), on different CD4+ T cell memory populations in ELCs and HIV-infected subjects with or without long-term cART. We found that the co-expression pattern of inhibitory receptors was significantly reduced in ELCs compared with HIV-1 cART-treated and viremic subjects, and similar to healthy controls. Markers associated with T cell exhaustion varied among different memory CD4+ T cell subsets and highest levels were found mainly on transitional memory T cells. CD4+ T cells co-expressing all inhibitory markers were positively correlated to T cell activation (CD38+ HLA-DR+) as well as the transcription factors Helios and FoxP3. Finally, clinical parameters such as CD4 count, HIV-1 viral load, and the CD4/CD8 ratio all showed significant associations with CD4+ T cell exhaustion. We demonstrate that ELCs are able to maintain lower levels of CD4+ T cell exhaustion despite years of ongoing viral replication compared with successfully cART-treated subjects. Our findings suggest that ELCs harbor a "healthy" state of inhibitory receptor expression on CD4+ T cells that might play part in maintenance of their control status.

Keywords: CD4+ T cells; CTLA-4; T cell exhaustion; TIGIT; elite controllers; human immunodeficiency virus type-1; inhibitory receptors; programmed cell death-1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ADP-ribosyl Cyclase 1 / biosynthesis
  • CD4 Lymphocyte Count
  • CD4-CD8 Ratio
  • CD4-Positive T-Lymphocytes / immunology*
  • CD8-Positive T-Lymphocytes / immunology*
  • CTLA-4 Antigen / biosynthesis
  • Forkhead Transcription Factors / biosynthesis
  • HIV-1 / immunology*
  • HLA-DR Antigens / biosynthesis
  • Humans
  • Ikaros Transcription Factor / biosynthesis
  • Immunologic Memory / immunology*
  • Lymphocyte Activation / immunology*
  • Membrane Glycoproteins / biosynthesis
  • Programmed Cell Death 1 Receptor / biosynthesis
  • Receptors, Immunologic / biosynthesis
  • Viral Load
  • Virus Replication

Substances

  • CTLA-4 Antigen
  • CTLA4 protein, human
  • FOXP3 protein, human
  • Forkhead Transcription Factors
  • HLA-DR Antigens
  • IKZF2 protein, human
  • Membrane Glycoproteins
  • PDCD1 protein, human
  • Programmed Cell Death 1 Receptor
  • Receptors, Immunologic
  • TIGIT protein, human
  • Ikaros Transcription Factor
  • CD38 protein, human
  • ADP-ribosyl Cyclase 1