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Preparation and Use of HIV-1 Infected Primary CD4+ T-Cells as Target Cells in Natural Killer Cell Cytotoxic Assays

Preparation and Use of HIV-1 Infected Primary CD4+ T-Cells as Target Cells in Natural Killer Cell Cytotoxic Assays

Published on: March 14, 2011

Aberrant natural killer (NK) cell activation and dysfunction among ART-treated HIV-infected adults in an African

Rose Nabatanzi¹, Lois Bayigga¹, Stephen Cose²

¹Department of Immunology and Molecular Biology, Makerere University College of Health Sciences, Kampala, Uganda.

Clinical Immunology (Orlando, Fla.)

|March 1, 2019

Abstract

Background:

We examined NK cell phenotypes and functions after seven years of ART and undetectable viral loads (<50 copies/ml) with restored CD4 T-cell counts (≥500 cells/μl) and age-matched healthy-HIV-uninfected individuals from the same community.

Methods:

Using flow-cytometry, NK cell phenotypes were described using lineage markers (CD56^+/-CD16^+/-). NK cell activation was determined by expression of activation receptors (NKG2D, NKp44 and NKp46) and activation marker CD69. NK cell function was determined by CD107a, granzyme-b, and IFN-gamma production.

Results:

CD56 dim and CD56 bright NK cells were lower among ART-treated-HIV-infected than among age-matched-HIV-negative individuals; p = 0.0016 and p = 0.05 respectively. Production of CD107a (P = 0.004) and Granzyme-B (P = 0.005) was lower among ART-treated-HIV-infected relative to the healthy-HIV-uninfected individuals. NKG2D and NKp46 were lower, while CD69 expression was higher among ART-treated-HIV-infected than healthy-HIV-uninfected individuals.

Conclusion:

NK cell activation and dysfunction persisted despite seven years of suppressive ART with "normalization" of peripheral CD4 counts.

Keywords:

107a Antiretroviral therapy Granzyme-B Interferon gamma NK Cytolytic function NK cell activation NK cell dysfunction NK degranulation NKG2D NKp46 Natural killer cells Sub-Saharan Africa

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