Effects of HIV infection and ART on phenotype and function of circulating monocytes, natural killer, and innate lymphoid
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AIDS Research and Therapy Open Access
REVIEW
Effects of HIV infection and ART on phenotype and function of circulating monocytes, natural killer, and innate lymphoid cells Rose Nabatanzi1* , Stephen Cose2, Moses Joloba1, Sarah Rowland Jones3 and Damalie Nakanjako4,5
Abstract HIV infection causes upregulation of markers of inflammation, immune activation and apoptosis of host adaptive, and innate immune cells particularly monocytes, natural killer (NK) and innate lymphoid cells (ILCs). Although antiretroviral therapy (ART) restores CD4 T-cell counts, the persistent aberrant activation of monocytes, NK and ILCs observed likely contributes to the incomplete recovery of T-cell effector functions. A better understanding of the effects of HIV infection and ART on the phenotype and function of circulating monocytes, NK, and ILCs is required to guide development of novel therapeutic interventions to optimize immune recovery. Keywords: HIV, Innate immunity, Monocytes, Natural killer cells, Innate lymphoid cells, Antiretroviral therapy Background The human innate immune system is comprised of a complex network of cellular and soluble proteins that work together to provide the first-line of defense against common invading pathogens prior to involvement of the adaptive immune response [1–3]. Innate immune cells including monocytes, natural killer cells (NK), innate lymphoid cells (ILCs), and other antigen presenting cells (APCs) play a crucial role in the ushering in the adaptive arm of the immune response [4, 5]. In particular, monocytes are precursor cells to professional APCs involved in immune surveillance [6]. In addition, they have patternrecognition receptors (PRRs) that detect conserved pathogen-associated molecular patterns (PAMPs) which lead to the induction of inflammatory responses that combat invading pathogens [7]. Natural killer cells produce cytokines; particularly interferon-gamma (IFN-ɣ) which activates phagocytic cells and primes APCs for interleukin 2 (IL-2) secretion thus shaping adaptive immunity *Correspondence: [email protected] 1 Department of Immunology and Molecular Biology, Makerere University College of Health Sciences, P. O. Box 7072, Kampala, Uganda Full list of author information is available at the end of the article
towards a T helper 1 (Th1) response [8, 9]. ILCs rapidly secrete immunoregulatory cytokines which makes them provide protective immunity early on during infection [10] and also maintain intestinal homeostasis by directly regulating T cells through the presentation of peptide antigens on major histocompatibility complex II [11]. During HIV infection, the adaptive immune system is directly affected through the rapid infection of CD4 T-cells [12] but the effects on the innate immune system are more indirect through microbial translocation, inflammation, and immune activation [13]. Immune activation and inflammation cause a reduction in the numbers of monocytes, NK and ILCs, consequently leading to poor innate and adaptive immune responses, all which result in suboptimal resp
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