Plasmacytoid Dendritic Cells Mediate Synergistic Effects of HIV and Lipopolysaccharide on CD27<sup>+</sup>IgD<sup>–</sup>Memory B Cell Apoptosis

Zhang, Lumin; Luo, Zhenwu; Sieg, Scott F.; Funderburg, Nicholas T.; Yu, Xiaojun; Fu, Pingfu; Wu, Hao; Jiao, Yanmei; Gao, Yong; Greenspan, Neil S.; Kilby, J. Michael; Li, Zihai; Lederman, Michael M.; Jiang, Wei

doi:10.1128/jvi.00682-14

Cited by 14 publications

(19 citation statements)

References 51 publications

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“…Indeed, our recent work shows that monocytes were activated in vivo in women compared to men, and plasma level of soluble CD14, a marker of monocyte activation by LPS, was higher in women relative to men [56], suggesting a role of systemic bacterial products in immune activation and inflammation. In addition, our recent studies have revealed that the heightened plasma level of LPS play an important role on T cell and B cell activation in HIV pathogenesis [57, 58]. Therefore, women should have overall higher levels of certain inflammation (e.g., sCD14) and increased proportions of activated monocyte subset (CD14−CD16+) compared to men [56].…”

Section: Discussionmentioning

confidence: 99%

Estrogen decreases tight junction protein ZO-1 expression in human primary gut tissues

Zhou

Zhang

Ding

et al. 2017

Clinical Immunology

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Females have a higher prevalence of most autoimmune diseases; however, the mechanism is unknown. In this study, we examined the expression of tight junction protein zonula occludens 1 (ZO-1) and estrogen receptor (ER)-α/β in human primary gut tissues by immunohistochemistry, immunofluorescence and qPCR. The expression of ZO-1 and ER-β but not ER-α was present in both male and female gut tissues. There was no sex difference in ER-β expression, but ZO-1 expression was decreased in females compared to males. In vitro, estrogen treatment decreased ZO-1 mRNA and protein expression, ZO-1 promoter activity, IL-6 production, and NF-κB activation in human primary gut tissues or the Caco-2 cells, but increased the ER-β expression in Caco-2 cells. Consistently, plasma IL-6 levels in females were reduced relative to males in vivo. Our finding indicates that estrogen may play a role in gut tight junction expression and permeability.

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Section: Discussionmentioning

confidence: 99%

Estrogen decreases tight junction protein ZO-1 expression in human primary gut tissues

Zhou

Zhang

Ding

et al. 2017

Clinical Immunology

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“…As such, this provides evidence that increased innate immune activation in patients could help account for heightened vaccine responses in patients. Of note, plasma level of bacterial 16S rDNA in aviremic and treated patients was lower than those observed in ART-naïve patients [33], and heightened microbial translocation has been shown to play a role in B cell dysfunction [43]. Whether intermediate levels of plasma microbial products promote B cell responses to vaccination in these patients or higher vaccine Ab responses in these patients reflect B cell polyrelativities is not known, and the exact mechanism requires further study.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous studies have shown that heightened microbial translocation plays a role in T cell and B cell activation in HIV disease [33][43]; therefore the level of microbial translocation was accessed in the current study. In addition, we performed comprehensive analyses of immune activation and potential correlates of immune responsiveness before and after influenza vaccination to determine whether serial annual vaccinations would uncover functional cellular or humoral differences between HIV-infected patients receiving successful ART and healthy HIV-negative volunteers.…”

Section: Introductionmentioning

confidence: 99%

Key differences in B cell activation patterns and immune correlates among treated HIV-infected patients versus healthy controls following influenza vaccination

Luo

Zhang

Martin

et al. 2016

Vaccine

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Background There is increasing recognition of the role of B cell dysfunction in HIV pathogenesis, but little is known about how these perturbations may influence responses to vaccinations. Methods Healthy controls (n = 16) and antiretroviral therapy (ART)-treated aviremic HIV-infected subjects (n = 26) receiving standard-of-care annual influenza vaccinations were enrolled in the present study. Total bacterial 16S rDNA levels were assessed by quantitative polymerase chain reactions in plasma. Serologic responses were characterized by ELISA, hemagglutination inhibition assay (HI), and microneutralization, and cell-mediated responses were assessed by ELISPOT (antigen-specific IgG+ antibody-secreting cells (ASCs)) and flow cytometry at pre-vaccination (D0), day 7-10 (D7) and day 14-21 (D14) post-vaccination. Results Decreased peripheral CD4+ T cell absolute counts and increased frequencies of cycling and apoptotic B cells were found at baseline in HIV-infected subjects relative to healthy controls. In healthy controls, post-vaccination neutralizing activities were related to the frequencies of vaccine-mediated apoptosis and cycling of B cells, but not to CD4+ T cell counts. In patients, both baseline and post-vaccination neutralizing activities were directly correlated with plasma level of bacterial 16S rDNA. However, overall vaccine responses including antibody titers and fold changes were comparable or greater in HIV-infected subjects relative to healthy controls. Conclusion B cell function correlates with measures of recall humoral immunity in response to seasonal influenza vaccination in healthy controls but not in ART-treated patients.

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“…Moreover, classical memory B cells are hyper-activated, characterized by highly spontaneous and activation-induced IgG secretion, and are prone to spontaneous apoptosis [17, 41, 53]. Fas (CD95) expression is up-regulated on memory B cells in HIV-infected patients, especially the HIV-viremic patients [17, 19, 20, 41, 54, 55]. Fas ligand may be up-regulated on memory B cells as well [17, 56].…”

Section: Mechanisms For the Loss Of Classical Memory B Cellsmentioning

confidence: 99%

HIV-associated memory B cell perturbations

Luo

Wan

et al. 2015

Vaccine

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Memory B-cell depletion, hyperimmunoglobulinemia, and impaired vaccine responses are the hallmark of B cell perturbations inhuman immunodeficiency virus (HIV) disease. Although B cells are not the targets for HIV infection, there is evidence for B cell, especially memory B cell dysfunction in HIV disease mediated by other cells or HIV itself. This review will focus on HIV-associated phenotypic and functional alterations in memory B cells. Additionally, we will discuss the mechanism underlying these perturbations and the effect of anti-retroviral therapy (ART) on these perturbations.

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Plasmacytoid Dendritic Cells Mediate Synergistic Effects of HIV and Lipopolysaccharide on CD27⁺IgD^–Memory B Cell Apoptosis

Cited by 14 publications

References 51 publications

Estrogen decreases tight junction protein ZO-1 expression in human primary gut tissues

Estrogen decreases tight junction protein ZO-1 expression in human primary gut tissues

Key differences in B cell activation patterns and immune correlates among treated HIV-infected patients versus healthy controls following influenza vaccination

HIV-associated memory B cell perturbations

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Plasmacytoid Dendritic Cells Mediate Synergistic Effects of HIV and Lipopolysaccharide on CD27+IgD–Memory B Cell Apoptosis

Cited by 14 publications

References 51 publications

Estrogen decreases tight junction protein ZO-1 expression in human primary gut tissues

Estrogen decreases tight junction protein ZO-1 expression in human primary gut tissues

Key differences in B cell activation patterns and immune correlates among treated HIV-infected patients versus healthy controls following influenza vaccination

HIV-associated memory B cell perturbations

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Plasmacytoid Dendritic Cells Mediate Synergistic Effects of HIV and Lipopolysaccharide on CD27⁺IgD^–Memory B Cell Apoptosis