Myeloid dendritic cells in HIV-1 infection

Derby, Nina; Martinelli, Elena; Robbiani, Melissa

doi:10.1097/coh.0b013e3283499d63

Cited by 22 publications

(27 citation statements)

References 67 publications

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“…NHP studies corroborate reports in HIV-infected patients showing that antiretroviral therapy restores mDCs and suggesting that direct killing of mDCs by the virus is a potential mechanism. mDCs can indeed be infected by HIV-1, the virus burden in mDCs isolated from chronically HIV-1-infected patients being considerable [15]. However, mDC depletion from circulation was also reported for HIV-2–infected patients and RMs infected with SIVmac (which is closely related to HIV-2), albeit mDCs appear to be less susceptible to HIV-2 infection [16], suggesting that additional factors may be responsible for mDC depletion.…”

Section: Introductionmentioning

confidence: 91%

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Kinetics of Myeloid Dendritic Cell Trafficking and Activation: Impact on Progressive, Nonprogressive and Controlled SIV Infections

Wijewardana

Kristoff

et al. 2013

PLoS Pathog

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We assessed the role of myeloid dendritic cells (mDCs) in the outcome of SIV infection by comparing and contrasting their frequency, mobilization, phenotype, cytokine production and apoptosis in pathogenic (pigtailed macaques, PTMs), nonpathogenic (African green monkeys, AGMs) and controlled (rhesus macaques, RMs) SIVagmSab infection. Through the identification of recently replicating cells, we demonstrated that mDC mobilization from the bone marrow occurred in all species postinfection, being most prominent in RMs. Circulating mDCs were depleted with disease progression in PTMs, recovered to baseline values after the viral peak in AGMs, and significantly increased at the time of virus control in RMs. Rapid disease progression in PTMs was associated with low baseline levels and incomplete recovery of circulating mDCs during chronic infection. mDC recruitment to the intestine occurred in all pathogenic scenarios, but loss of mucosal mDCs was associated only with progressive infection. Sustained mDC immune activation occurred throughout infection in PTMs and was associated with increased bystander apoptosis in blood and intestine. Conversely, mDC activation occurred only during acute infection in nonprogressive and controlled infections. Postinfection, circulating mDCs rapidly became unresponsive to TLR7/8 stimulation in all species. Yet, stimulation with LPS, a bacterial product translocated in circulation only in SIV-infected PTMs, induced mDC hyperactivation, apoptosis and excessive production of proinflammatory cytokines. After infection, spontaneous production of proinflammatory cytokines by mucosal mDCs increased only in progressor PTMs. We thus propose that mDCs promote tolerance to SIV in the biological systems that lack intestinal dysfunction. In progressive infections, mDC loss and excessive activation of residual mDCs by SIV and additional stimuli, such as translocated microbial products, enhance generalized immune activation and inflammation. Our results thus provide a mechanistic basis for the role of mDCs in the pathogenesis of AIDS and elucidate the causes of mDC loss during progressive HIV/SIV infections.

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Section: Introductionmentioning

confidence: 91%

“…To date, all information on mDCs in HIV/SIV infections is derived from studies performed on persistent progressive (pathogenic) infections (reviewed in [15]). Very few of these studies focused on mDCs at mucosal sites [57]–[60].…”

Section: Introductionmentioning

confidence: 99%

Kinetics of Myeloid Dendritic Cell Trafficking and Activation: Impact on Progressive, Nonprogressive and Controlled SIV Infections

Wijewardana

Kristoff

et al. 2013

PLoS Pathog

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“…Myeloid DCs are especially important in relation to HIV-1 infection and host defense (8). In the current study, immune responses elicited in human myeloid DCs stimulated with the recombinant lactobacilli were analyzed.…”

Section: Discussionmentioning

confidence: 99%

Construction and Immunological Evaluation of Dual Cell Surface Display of HIV-1 Gag and Salmonella enterica Serovar Typhimurium FliC in Lactobacillus acidophilus for Vaccine Delivery

Kajikawa

Zhang

Long

et al. 2012

Clin Vaccine Immunol

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ABSTRACTOral vaccines that elicit a mucosal immune response may be effective against human immunodeficiency virus type 1 (HIV-1) because its transmission occurs mainly at the mucosa. The aim of this study was to construct recombinantLactobacillusfor oral delivery of oral vaccines against HIV-1 and to evaluate their immunogenicity. A recombinantLactobacillus acidophilusstrain expressing the HIV-1 Gag on the bacterial cell surface was established by fusion with the signal peptide and anchor motif of a mucus binding protein (Mub) fromL. acidophiluswith or without coexpression ofSalmonella entericaserovar Typhimurium flagellin (FliC) fused to a different Mub signal peptide and anchor. Using HEK293 cells engineered to express Toll-like receptor 5 (TLR5), the biological activity of FliC on the bacterial cell surfaces was determined. The surface-exposed flagellin retained its TLR5-stimulating activity, suggesting that the recombinant strain with Gag and FliC dual display might provide a different immunopotency than the strain expressing only Gag. The immunological properties of the recombinant strains were assessed by coculture with human myeloid dendritic cells (DCs). The heterologous antigens on the cell surface affected maturation and cytokine responses of DCs. Acquired immune responses were also investigated by intragastric immunization of mice. The enzyme-linked immunosorbent spot assay showed induction of gamma interferon-producing cells at local mucosa after immunization of mice with the Gag-producing strain. Meanwhile, the immunization withL. acidophilusdisplaying both Gag and FliC resulted in an increase of Gag-specific IgA-secreting cells. These results suggested that the Gag-displayingL. acidophiluselicited specific immune responses and the coexistence of FliC conferred an adjuvant effect on local IgA production.

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“…There, DCs are one of the earliest cell types to be exposed to the virus and present an inherent capacity to orchestrate a homeostatic balance between tolerance and protection [1–4]. It is likely that the incapacity to keep a balance in these homeostatic processes will promote inflammation and lead to disease progression [5].…”

Section: Introductionmentioning

confidence: 99%

Influence of Dendritic Cells on B-Cell Responses during HIV Infection

Poudrier

Chagnon-Choquet

Roger

2012

Clinical and Developmental Immunology

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Dendritic cells (DCs) modulate B-cell differentiation, activation, and survival mainly through production of growth factors such as B lymphocyte stimulator (BLyS/BAFF). DC populations have been reported to be affected in number, phenotype and function during HIV infection and such alterations may contribute to the dysregulation of the B-cell compartment. Herein, we reflect on the potential impact of DC on the pathogenesis of HIV-related B cell disorders, and how DC status may modulate the outcome of mucosal B cell responses against HIV, which are pivotal to the control of disease. A concept that could be extrapolated to the overall outcome of HIV disease, whereby control versus progression may reside in the host’s capacity to maintain DC homeostasis at mucosal sites, where DC populations present an inherent capacity of modulating the balance between tolerance and protection, and are amongst the earliest cell types to be exposed to the virus.

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Myeloid dendritic cells in HIV-1 infection

Cited by 22 publications

References 67 publications

Kinetics of Myeloid Dendritic Cell Trafficking and Activation: Impact on Progressive, Nonprogressive and Controlled SIV Infections

Kinetics of Myeloid Dendritic Cell Trafficking and Activation: Impact on Progressive, Nonprogressive and Controlled SIV Infections

Construction and Immunological Evaluation of Dual Cell Surface Display of HIV-1 Gag and Salmonella enterica Serovar Typhimurium FliC in Lactobacillus acidophilus for Vaccine Delivery

Influence of Dendritic Cells on B-Cell Responses during HIV Infection

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