Blood Dendritic Cells Interact with Splenic Marginal Zone B Cells to Initiate T-Independent Immune Responses

Balázs, Mercedesz; Martin, Flavius; Zhou, Tong; Kearney, John F.

doi:10.1016/s1074-7613(02)00389-8

Cited by 549 publications

(488 citation statements)

References 36 publications

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“…injection of particulate Ag (20). We found increased expression of syndecan I on WT MZB cells as early as 16 h after infection, but by 24 h, this marker was no longer detected (Fig.…”

Section: B Hermsii Infection Activates Mzb Cellsmentioning

confidence: 70%

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Infection-Induced Marginal Zone B Cell Production of Borrelia hermsii-Specific Antibody Is Impaired in the Absence of CD1d

Belperron

Dailey

Bockenstedt

2005

The Journal of Immunology

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Ab that arise in the absence of T cell help are a critical host defense against infection with the spirochetes Borrelia burgdorferi and Borrelia hermsii. We have previously shown that CD1d-deficient (CD1d−/−) mice have impaired resistance to infection with B. burgdorferi. In mice, CD1d expression is highest on marginal zone B (MZB) cells, which produce Ab to blood-borne Ag. In this study we examined MZB cell activation and Ab production in mice infected with B. hermsii, which achieve high levels of bacteremia. We show by flow cytometry that MZB cells associate with B. hermsii and up-regulate the activation markers syndecan I and B7.1 within 16 h of infection. By 24 h, MZB cells secrete B. hermsii-specific IgM, coinciding with the loss of activation marker expression and the reduction in spirochete burden. In contrast, MZB cells from CD1d−/− mice remain activated for at least 96 h of infection, but produce only minimal B. hermsii-specific IgM in vivo and ex vivo; pathogen burden in the blood also remains elevated. Wild-type mice depleted of MZB cells using mAb to LFA-1 and α4β1 integrin have reduced serum levels of B. hermsii-specific IgM and increased pathogen burden, similar to B. hermsii-infected CD1d−/− mice. Passive transfer of immune mouse serum, but not naive mouse serum, into infected CD1d−/− mice leads to down-regulation of activation markers and clearance of B. hermsii from the MZB cells. These results demonstrate that blood-borne spirochetes activate MZB cells to produce pathogen-specific IgM and reveal a role for CD1d in this process.

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“…injection of particulate Ag (20). We found increased expression of syndecan I on WT MZB cells as early as 16 h after infection, but by 24 h, this marker was no longer detected (Fig.…”

Section: B Hermsii Infection Activates Mzb Cellsmentioning

confidence: 70%

“…Dendritic cells can capture Ag and transport them to the spleen where they interact with MZB cells to initiate T-independent immune responses (20). However, marginal zone macrophages probably play a lesser role, because their depletion has been shown to increase humoral responses to TI-2 Ag (9).…”

Section: Discussionmentioning

confidence: 99%

Infection-Induced Marginal Zone B Cell Production of Borrelia hermsii-Specific Antibody Is Impaired in the Absence of CD1d

Belperron

Dailey

Bockenstedt

2005

The Journal of Immunology

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“…These findings suggest that BAFF may be produced by DC and other cells in response to pathogens to promote rapid production of protective Ab. Indeed, Balazs et al [14] found that the rapid Ab response to S. pneumoniae in mice is mediated by blood DC, which bind bacteria, migrate to splenic marginal zones (MZ) and promote antigen-specific MZ B cell Ab production through a BAFF-dependent mechanism. Consistent with this model, we and others have found that mouse and human DC promote B cell proliferation in vitro by secreting BAFF.…”

Section: Introductionmentioning

confidence: 99%

BAFF and LPS cooperate to induce B cells to become susceptible to CD95/Fas‐mediated cell death

et al. 2007

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Microorganisms with pathogen-associated molecular patterns (PAMP) activate B cells directly by binding to TLR and also indirectly by inducing APC to release cytokines such as BAFF that promote B cell survival. We found that murine B cells activated concomitantly with LPS (TLR-4 ligand) and BAFF are protected from spontaneous apoptosis, but are more susceptible to Fas/CD95-mediated cell death. This increased susceptibility to Fas-induced apoptosis is associated with a dramatic coordinated upregulation of Fas/CD95 and IRF-4 expression through a mechanism mediated, at least in part, by inhibition of the MEK/ERK pathway.

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“…In other studies, DC-derived cytokines also promoted B cell proliferation and switching to IgA, independent of CD40; however, this was mediated through BAFF and APRIL (17,18), which also support plasmablast survival in vivo (19). The kinetics of the response suggest that DC-derived IFN-b and TNF-a play important roles in the early phase of humoral immunity.…”

Section: Discussionmentioning

confidence: 76%

“…This is important for the development of safe and efficient vaccination strategies that reduce the burden of C. jejuni-induced disease, including the development of serious sequelae like GBS. Because myeloid cells, such as DCs, are important for bridging innate and adaptive immunity, as well as play an important role in the development of humoral immunity to T-independent Ags (17)(18)(19), we previously investigated the potential of DCs stimulated with C. jejuni LOS to promote B cell responses. It was shown that human monocyte-derived DCs stimulated with C. jejuni LOS produce soluble factors that enhance B cell proliferation, independently of T cells (14).…”

mentioning

confidence: 99%

Sialylation of Campylobacter jejuni Endotoxin Promotes Dendritic Cell–Mediated B Cell Responses through CD14-Dependent Production of IFN-β and TNF-α

Huizinga

Rijs

Bajramović

et al. 2013

The Journal of Immunology

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Campylobacter jejuni is the most common bacterial cause of human gastroenteritis and often precedes development of Guillain–Barré syndrome (GBS), a life-threatening paralytic disease. The incorporation of the carbohydrate sialic acid into C. jejuni lipooligosaccharides (LOS) is associated with increased severity of gastroenteritis and with induction of GBS; however, the underlying mechanisms remain completely unknown. In this study, we demonstrate that sialic acids in C. jejuni endotoxin enhance the rapid production of IFN-β and TNF-α by human dendritic cells (DCs). Using neutralizing Abs and receptors it was shown that these DC-derived cytokines promote the proliferation of human mucosal B cells in a T cell–independent manner. The production of both IFN-β and TNF-α by DCs in response to LOS requires CD14, and the amplified response of DCs to sialylated C. jejuni LOS is CD14 dependent. Together, these results indicate that sialylation of C. jejuni LOS increases DC activation and promotes subsequent B cell responses through CD14-driven production of IFN-β and TNF-α. This enhanced DC/B cell response may explain the increased pathogenicity of sialylated C. jejuni and may be key to the initiation of B cell–mediated autoimmunity in GBS.

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Blood Dendritic Cells Interact with Splenic Marginal Zone B Cells to Initiate T-Independent Immune Responses

Cited by 549 publications

References 36 publications

Infection-Induced Marginal Zone B Cell Production of Borrelia hermsii-Specific Antibody Is Impaired in the Absence of CD1d

Infection-Induced Marginal Zone B Cell Production of Borrelia hermsii-Specific Antibody Is Impaired in the Absence of CD1d

BAFF and LPS cooperate to induce B cells to become susceptible to CD95/Fas‐mediated cell death

Sialylation of Campylobacter jejuni Endotoxin Promotes Dendritic Cell–Mediated B Cell Responses through CD14-Dependent Production of IFN-β and TNF-α

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