HIV Nef Expression Favors the Relative Preservation of CD4+ T Regulatory Cells That Retain Some Important Suppressive Functions

Chrobák, Pavel; Afkhami, Soheila; Priceputu, Elena; Poudrier, Johanne; Meunier, Clémence; Hanna, Zaher; Sparwasser, Tim; Jolicoeur, Paul

doi:10.4049/jimmunol.1203272

Cited by 6 publications

(3 citation statements)

References 63 publications

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“…Although depleted in absolute numbers, the proportion of Tregs relative to total CD4+ cells was enhanced in Tg compared to non-Tg mice. This Treg enrichment is the direct result of HIV-1 Nef expression in CD4+ T-cells, occurs independently of Nef-induced lymphopenia, and involves multiple mechanisms: lower apoptosis, enhanced cell division, and increased generation from precursors [ 55 ]. Consistent with our findings, studies in HIV-infected patients have also reported a relative increase in frequency but reduced absolute numbers of Tregs [ 56 - 60 ].…”

Section: Discussionmentioning

confidence: 99%

Defective IL-17- and IL-22-dependent mucosal host response to Candida albicans determines susceptibility to oral candidiasis in mice expressing the HIV-1 transgene

et al. 2014

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BackgroundThe tissue-signaling cytokines IL-17 and IL-22 are critical to host defense against oral Candida albicans infection, by their induction of oral antimicrobial peptide expression and recruitment of neutrophils. Mucosal Th17 cells which produce these cytokines are preferentially depleted in HIV-infected patients. Here, we tested the hypothesis that defective IL-17- and IL-22-dependent host responses to C. albicans determine the phenotype of susceptibility to oropharyngeal candidiasis (OPC) in transgenic (Tg) mice expressing HIV-1.ResultsNaïve CD4+ T-cells and the differentiated Th1, Th2, Th17, Th1Th17 and Treg lineages were all profoundly depleted in cervical lymph nodes (CLNs) of these Tg mice. However, naive CD4+ cells from Tg mice maintained the capacity to differentiate into these lineages in response to polarizing cytokines in vitro. Expression of Il17, Il22, S100a8 and Ccl20 was enhanced in oral mucosal tissue of non-Tg, but not of Tg mice, after oral infection with C. albicans. Treatment of infected Tg mice with the combination of IL-17 and IL-22, but not IL-17 or Il-22 alone, significantly reduced oral burdens of C. albicans and abundance of Candida hyphae in the epithelium of tongues of infected Tg mice, and restored the ability of the Tg mice to up-regulate expression of S100a8 and Ccl20 in response to C. albicans infection.ConclusionsThese findings demonstrate that defective IL-17- and IL-22-dependent induction of innate mucosal immunity to C. albicans is central to the phenotype of susceptibility to OPC in these HIV transgenic mice.Electronic supplementary materialThe online version of this article (doi:10.1186/s12865-014-0049-9) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Defective IL-17- and IL-22-dependent mucosal host response to Candida albicans determines susceptibility to oral candidiasis in mice expressing the HIV-1 transgene

et al. 2014

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“…Increased expression of IDO promotes the differentiation of naive CD4 + T cells into Tregs . On the other hand, Tregs also appear to be less prone to HIV‐induced apoptosis . It was suggested that in HIV infection, IL‐21 increased the relative number of Tregs by reducing the apoptosis of Tregs and promoting their survival .…”

Section: Treg and Th17 Cells In Hiv Infectionmentioning

confidence: 99%

Regulatory T cells and T helper 17 cells in viral infection

et al. 2020

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CD4 + T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4 + T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection. How to cite this article: Wan Z, Zhou Z, Liu Y, et al. Regulatory T cells and T helper 17 cells in viral infection. Scand J Immunol. 2020;91:e12873.

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“…Absolute Treg numbers are decreased in the circulation in both acute and chronically infected individuals however, the percentage of Tregs in chronic infection is relatively increased ( 150 , 151 ). The percentage increase in chronically infected individuals may be attributed to an increase in proliferation or it may be that these cells are relatively resistant to HIV-associated cell death ( 152 ). The increase in percentage of Tregs means that unlike CD4+ T cells which rapidly decline in HIV infection, Tregs appear to be relatively spared.…”

Section: Decidual Immune Cells Preterm Birth and Hivmentioning

confidence: 99%

Preterm Birth in Women With HIV: The Role of the Placenta

Ikumi

Matjila

2022

Front. Glob. Womens Health

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Maternal HIV infection is associated with an increased risk of preterm birth (PTB). However, the mechanisms underlying this increased risk in women with HIV remain poorly understood. In this regard, it is well-established that labor is an inflammatory process and premature activation of the pro-inflammatory signals (associated with labor) can result in preterm labor which can subsequently lead to PTB. HIV infection is known to cause severe immune dysregulation within its host characterized by altered immune profiles, chronic inflammation and eventually, the progressive failure of the immune system. The human placenta comprises different immune cell subsets, some of which play an important role during pregnancy including participating in the inflammatory processes that accompany labor. It is therefore plausible that HIV/antiretroviral therapy (ART)-associated immune dysregulation within the placental microenvironment may underlie the increased risk of PTB reported in women with HIV. Here, we review evidence from studies that point toward the placental origin of spontaneous PTB and discuss possible ways maternal HIV infection and/or ART could increase this risk. We focus on key cellular players in the maternal decidua including natural killer cells, CD4+ T cells including CD4+ regulatory T cells, CD8+ T cells as well as macrophages.

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HIV Nef Expression Favors the Relative Preservation of CD4+ T Regulatory Cells That Retain Some Important Suppressive Functions

Cited by 6 publications

References 63 publications

Defective IL-17- and IL-22-dependent mucosal host response to Candida albicans determines susceptibility to oral candidiasis in mice expressing the HIV-1 transgene

Defective IL-17- and IL-22-dependent mucosal host response to Candida albicans determines susceptibility to oral candidiasis in mice expressing the HIV-1 transgene

Regulatory T cells and T helper 17 cells in viral infection

Preterm Birth in Women With HIV: The Role of the Placenta

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