Characteristics of Natural Killer Cells in Malaysian HIV Patients Presenting with Immune Restoration Disease After ART
- *Corresponding Author:
- Dr. Dino Bee Aik Tan
School of Pathology and Laboratory Medicine
University of Western Australia, Level 2
Medical Research Foundation Building
Royal Perth Hospital, Rear of 50 Murray Street
Perth, WA 6000, Australia
E-mail: [email protected]
Received Date: October 03, 2010; Accepted Date: October 15, 2010; Published Date: October 18, 2010
Citation: Tan DBA, Yong YK, Tan HY, French M, Kamarulzaman A, et al. (2010) Characteristics of Natural Killer Cells in Malaysian HIV Patients Presenting with Immune Restoration Disease After ART. J AIDS Clinic Res 1: 102 doi: 10.4172/2155-6113.1000102
Copyright: © 2010 Tan DBA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objectives: Natural killer (NK) cell function was investigated in Malaysian HIV patients beginning antiretroviral therapy (ART) with advanced immunodeficiency. Some patients experienced immune restoration disease (IRD) presenting as exacerbations of pre-existing infections. Whilst most IRD are attributed to interferon-gamma (IFN?) produced by T-cells, NK cells may also contribute. Methods: Blood leukocytes were collected prospectively from 100 HIV patients over 1 year on ART, plus 36 healthy controls. Eleven patients who experienced an IRD and 14 matched controls were assayed. Cells producing IFN? were quantitated by ELISpot after stimulation with an NK target (K562 cells) or antigens from pathogens associated with the IRD. NK cell subsets, CD16 and perforin expression were determined by flow cytometry Results: NK cell IFN? responses were lower in HIV patients at baseline (p<0.001), improved by Week 24 (p<0.01) but remained lower than uninfected controls (p<0.05). Proportions of CD56hi NK cells increased (p<0.01) above controls at Week 24. Perforin expression on these cells was higher than controls at baseline (p<0.01), but declined on ART. Proportions of CD56hl NK cells were similar in patients and controls throughout. IRD patients showed lower CD16 expression on CD56lo NK cells than non-IRD patients before treatment (p<0.05) Conclusions: NK cells profiles were restored on ART, but NK cell IFN? production remained impaired. Low CD16 expression on CD56lo NK cells may mark a predisposition for an IRD.