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CD56negCD16? NK cells are activated mature NK cells with impaired effector function during HIV-1 infection.

ABSTRACT: A subset of CD3(neg)CD56(neg)CD16? Natural Killer (NK) cells is highly expanded during chronic HIV-1 infection. The role of this subset in HIV-1 pathogenesis remains unclear. The lack of NK cell lineage-specific markers has complicated the study of minor NK cell subpopulations.Using CD7 as an additional NK cell marker, we found that CD3(neg)CD56(neg)CD16? cells are a heterogeneous population comprised of CD7? NK cells and CD7(neg) non-classical myeloid cells. CD7?CD56(neg)CD16? NK cells are significantly expanded in HIV-1 infection. CD7?CD56(neg)CD16? NK cells are mature and express KIRs, the C-type lectin-like receptors NKG2A and NKG2C, and natural cytotoxicity receptors similar to CD7?CD56?CD16? NK cells. CD7?CD56(neg) NK cells in healthy donors produced minimal IFN? following K562 target cell or IL-12 plus IL-18 stimulation; however, they degranulated in response to K562 stimulation similar to CD7?CD56? NK cells. HIV-1 infection resulted in reduced IFN? secretion following K562 or cytokine stimulation by both NK cell subsets compared to healthy donors. Decreased granzyme B and perforin expression and increased expression of CD107a in the absence of stimulation, particularly in HIV-1-infected subjects, suggest that CD7?CD56(neg)CD16? NK cells may have recently engaged target cells. Furthermore, CD7?CD56(neg)CD16? NK cells have significantly increased expression of CD95, a marker of NK cell activation.Taken together, CD7?CD56(neg)CD16? NK cells are activated, mature NK cells that may have recently engaged target cells.

SUBMITTER: Milush JM

PROVIDER: S-EPMC3892122 | biostudies-literature | 2013 Dec

REPOSITORIES: biostudies-literature

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CD56negCD16⁺ NK cells are activated mature NK cells with impaired effector function during HIV-1 infection.

Milush Jeffrey M JM López-Vergès Sandra S York Vanessa A VA Deeks Steven G SG Martin Jeffrey N JN Hecht Frederick M FM Lanier Lewis L LL Nixon Douglas F DF

Retrovirology 20131218

<h4>Background</h4>A subset of CD3(neg)CD56(neg)CD16⁺ Natural Killer (NK) cells is highly expanded during chronic HIV-1 infection. The role of this subset in HIV-1 pathogenesis remains unclear. The lack of NK cell lineage-specific markers has complicated the study of minor NK cell subpopulations.<h4>Results</h4>Using CD7 as an additional NK cell marker, we found that CD3(neg)CD56(neg)CD16⁺ cells are a heterogeneous population comprised of CD7⁺ NK cells and CD7(neg) non-classical myeloid cells. C ...[more]

PMID: 24351015

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Project description:ObjectivesThree decades after HIV recognition and its association with AIDS development, many advances have emerged - especially related to prevention and treatment. Undoubtedly, the development of Highly Active Antiretroviral Therapy (HAART) dramatically changed the future of the syndrome that we know today. In the present study, we evaluate the impact of Highly Active Antiretroviral Therapy on macrophage function and its relevance to HIV pathogenesis.MethodsPBMCs were isolated from blood samples and monocytes (CD14+ cells) were purified. Monocyte-Derived Macrophages (MDMs) were activated on classical (MGM-CSF+IFN-γ) or alternative (MIL-4+IL13) patterns using human recombinant cytokines for six days. After this period, Monocyte-Derived Macrophages were stimulated with TLR2/Dectin-1 or TLR4 agonists and we evaluated the influence of HIV-1 infection and Highly Active Antiretroviral Therapy on the release of cytokines/chemokines by macrophages.ResultsThe data were obtained using Monocyte-Derived Macrophages derived from HIV naïve or from patients on regular Highly Active Antiretroviral Therapy. Classically Monocyte-Derived Macrophages obtained from HIV-1 infected patients on Highly Active Antiretroviral Therapy released higher levels of IL-6 and IL-12 even without PAMPs stimuli when compared to control group. On the other hand, alternative Monocyte-Derived Macrophages derived from HIV-1 infected patients on Highly Active Antiretroviral Therapy released lower levels of IL-6, IL-10, TNF-α, IP-10 and RANTES after LPS stimuli when compared to control group. Furthermore, healthy individuals have a complex network of cytokines/chemokines released by Monocyte-Derived Macrophages after PAMP stimuli, which was deeply affected in MDMs obtained from naïve HIV-1 infected patients and only partially restored in MDMs derived from HIV-1 infected patients even on regular Highly Active Antiretroviral Therapy.ConclusionOur therapy protocols were not effective in restoring the functional alterations induced by HIV, especially those found on macrophages. These findings indicate that we still need to develop new approaches and improve the current therapy protocols, focusing on the reestablishment of cellular functions and prevention/treatment of opportunistic infections.

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CD56negCD16? NK cells are activated mature NK cells with impaired effector function during HIV-1 infection.

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CD56negCD16⁺ NK cells are activated mature NK cells with impaired effector function during HIV-1 infection.

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