B Cell Maintenance of Subcapsular Sinus Macrophages Protects against a Fatal Viral Infection Independent of Adaptive Immunity

Moseman, E. Ashley; Iannacone, Matteo; Bosurgi, Lidia; Tonti, Elena; Chevrier, Nicolas; Tumanov, Alexei V.; Fu, Yang–Xin; Hacohen, Nir; Andrian, Ulrich H. von

doi:10.1016/j.immuni.2012.01.013

Cited by 140 publications

(173 citation statements)

References 55 publications

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“…Indeed B-cell tropism requires passage through a myeloid cell . However Bcells influence myeloid function (You et al, 2011;Moseman et al, 2012); B-cell-derived IgM promotes early antigen capture (Heyman, 2014), and B-cells transport antigens from myeloid cells into LN and splenic follicles (Phan et al, 2007;Cinamon et al, 2008). Therefore, B-cell deficiency could compromise MuHV-4 spread indirectly by compromising myeloid infection.…”

mentioning

confidence: 99%

B-cell-independent lymphoid tissue infection by a B-cell-tropic rhadinovirus

Chao

Frederico

Stevenson

2015

Journal of General Virology

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confidence: 99%

B-cell-independent lymphoid tissue infection by a B-cell-tropic rhadinovirus

Chao

Frederico

Stevenson

2015

Journal of General Virology

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“…Moreover, it has been shown that lymphotoxins are derived from B cells, which are important for maintenance of CD169 ϩ cells (29,39). Consistently, BAFFR-deficient animals exhibited lower lymphotoxin alpha (Lt␣) and lymphotoxin beta (Lt␤) expression levels than their corresponding controls (Fig.…”

Section: Baffr Deficiency Results In Reduced B Cell-mediated Maintenamentioning

confidence: 55%

“…Lymphotoxin signaling is critical for CD169 ϩ cell development in spleen and lymph node tissues (32,38,39,41). Moreover, it has been shown that lymphotoxins are derived from B cells, which are important for maintenance of CD169 ϩ cells (29,39).…”

Section: Baffr Deficiency Results In Reduced B Cell-mediated Maintenamentioning

confidence: 99%

Deficiency of the B Cell-Activating Factor Receptor Results in Limited CD169+ Macrophage Function during Viral Infection

Huang²,

Häussinger

et al. 2015

Z Gastroenterol

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The B cell-activating factor (BAFF) is critical for B cell development and humoral immunity in mice and humans. While the role of BAFF in B cells has been widely described, its role in innate immunity remains unknown. Using BAFF receptor (BAFFR)-deficient mice, we characterized BAFFR-related innate and adaptive immune functions following infection with vesicular stomatitis virus (VSV) and lymphocytic choriomeningitis virus (LCMV). We identified a critical role for BAFFR signaling in the generation and maintenance of the CD169 ؉ macrophage compartment. Consequently, Baffr ؊/؊ mice exhibited limited induction of innate type I interferon production after viral infection. Lack of BAFFR signaling reduced virus amplification and presentation following viral infection, resulting in highly reduced antiviral adaptive immune responses. As a consequence, BAFFR-deficient mice showed exacerbated and fatal disease after viral infection. Mechanistically, transient lack of B cells in Baffr ؊/؊ animals resulted in limited lymphotoxin expression, which is critical for maintenance of CD169 ؉ cells. In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections. IMPORTANCEViruses cause acute and chronic infections in humans resulting in millions of deaths every year. Innate immunity is critical for the outcome of a viral infection. Innate type I interferon production can limit viral replication, while adaptive immune priming by innate immune cells induces pathogen-specific immunity with long-term protection. Here, we show that BAFFR deficiency not only perturbed B cells, but also resulted in limited CD169 ؉ macrophages. These macrophages are critical in amplifying viral particles to trigger type I interferon production and initiate adaptive immune priming. Consequently, BAFFR deficiency resulted in reduced enforced viral replication, limited type I interferon production, and reduced adaptive immunity compared to BAFFRcompetent controls. As a result, BAFFR-deficient mice were predisposed to fatal viral infections. Thus, BAFFR expression is critical for innate immune activation and antiviral immunity.

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“…recently, it has been shown that B cells are important for proper innate antiviral responses by controlling macrophage maintenance and production of type I IFns upon vsv infection [49]. also, B cells seem to play a pivotal role during innate responses to systemic infections.…”

mentioning

confidence: 99%

“…also, B cells seem to play a pivotal role during innate responses to systemic infections. Kelly-scumpia et al [49,50] have demonstrated that during bacterial sepsis, type-I-IFn-mediated activation of marginal zone and follicular B cells contributed to early chemokine production and to improved survival rates. thus, these two studies have identified a novel protective role for type I IFn and B cells during early immune responses to viral and systemic infections.…”

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confidence: 99%

Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice

Costa

Fagundes

Valadão

et al. 2014

Med Microbiol Immunol

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cells play a pivotal role in host responses against primary Denv infection in mice. after infection, μMt −/− mice showed increased viral loads followed by severe disease manifestation characterized by intense thrombocytopenia, hemoconcentration, cytokine production and massive liver damage that culminated in death. In addition, we show that poly and monoclonal anti-Denv-specific antibodies can sufficiently increase viral replication through a suppression of early innate antiviral responses and enhance disease manifestation, so that a mostly non-lethal illness becomes a fatal disease resembling human DHF/Dss. Finally, treatment with intravenous immunoglobulin containing anti-Denv antibodies confirmed the potential enhancing capacity of Abstract Dengue is a mosquito-borne disease caused by one of four serotypes of Dengue virus (Denv-1-4). epidemiologic and observational studies demonstrate that the majority of severe dengue cases, dengue hemorrhagic fever and dengue shock syndrome (DHF/Dss), occurs predominantly in either individuals with cross-reactive immunity following a secondary heterologous infection or in infants with primary Denv infections born from dengue-immune mothers, suggesting that B-cell-mediated and antibody responses impact on disease evolution. We demonstrate here that B Electronic supplementary material the online version of this article

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B Cell Maintenance of Subcapsular Sinus Macrophages Protects against a Fatal Viral Infection Independent of Adaptive Immunity

Cited by 140 publications

References 55 publications

B-cell-independent lymphoid tissue infection by a B-cell-tropic rhadinovirus

B-cell-independent lymphoid tissue infection by a B-cell-tropic rhadinovirus

Deficiency of the B Cell-Activating Factor Receptor Results in Limited CD169+ Macrophage Function during Viral Infection

Subversion of early innate antiviral responses during antibody-dependent enhancement of Dengue virus infection induces severe disease in immunocompetent mice

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