Type I IFN Signaling on Both B and CD4 T Cells Is Required for Protective Antibody Response to Adenovirus

Zhu, Jia; Huang, Xin; Yang, Yiping

doi:10.4049/jimmunol.178.6.3505

Cited by 53 publications

(64 citation statements)

References 32 publications

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“…injection of the Ad vectors (31), whereas type I IFN was undetectable even at 6 h after injection (30). Zhu et al (32) reported a maximum time point for the detection of type I IFN production at 12 h after i.v. injection of Ad vectors.…”

Section: Discussionmentioning

confidence: 99%

Induction of type I interferon by adenovirus-encoded small RNAs

Yamaguchi

Kono

Kouyama

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Transduction with replication-incompetent recombinant adenovirus (Ad) vectors results in a rapid activation of innate immune responses, such as inflammatory cytokine production and subsequent tissue damage. The precise mechanisms of the innate immune responses induced by Ad vectors remain to be clarified. Possible components of Ad vectors that activate innate immune responses are the capsid protein, the viral genome (DNA), and viral transcripts. In the present study, we demonstrate that virus-associated RNAs (VA-RNAs), which are small RNAs transcribed by RNA polymerase III, induce the production of type I IFN (IFN-α and IFN-β), but they do not induce the production of inflammatory cytokines (IL-6 and IL-12), in mouse embryonic fibroblasts (MEFs) and granulocyte-macrophage colony-stimulating factor–generated bone marrow-derived dendritic cells (GM-DCs). We also show that IFN-β promoter stimulator-1 is involved in VA-RNA–dependent IFN-β production in MEFs and is partially involved in type I IFN production in GM-DCs. This study provides important insight into the mechanisms of Ad vector-triggered innate immune responses, which may lead to more advanced and rational Ad vector designs for gene therapies and vaccine applications.

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Section: Discussionmentioning

confidence: 99%

Induction of type I interferon by adenovirus-encoded small RNAs

Yamaguchi

Kono

Kouyama

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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“…[75][76][77][78] B cells are also known targets of type I interferons: IFN-␣/␤ was reported to inhibit B cell lymphopoiesis, 79 to induce B cells in a state of partial activation, 80 to promote plasma cell differentiation, 81 and to stimulate the antibody response and the isotype switching in B cells in response to antigens. [82][83][84] Furthermore, the production of B-cell-activating factor by epithelial cells or DCs was found to be induced by IFN-␤ or IFN-␣. 85,86 The present study provides the first evidence that IFN-␣/␤ influences the development of Bartonella-induced lymphadenopathy.…”

Section: Mechanism Leading To Lymphadenopathy In Bartonella-infected mentioning

confidence: 99%

Lymphadenopathy in a Novel Mouse Model of Bartonella-Induced Cat Scratch Disease Results from Lymphocyte Immigration and Proliferation and Is Regulated by Interferon-α/β

Kunz

Oberle

Sander

et al. 2008

The American Journal of Pathology

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In immunocompetent humans, cat scratch disease (CSD) is elicited by the Gram-negative bacterium Bartonella henselae and is characterized by a benign regional lymphadenopathy, the pathogenesis of which is poorly understood. Here, we describe a novel mouse model of Bartonella-induced CSD-like disease that allowed us to investigate the mechanisms leading to lymphadenopathy in vivo. In wild-type mice, a subcutaneous inoculation of either viable or inactivated B. henselae led to a strong swelling of the draining lymph node, which was long-lasting despite the rapid elimination of the bacteria. Carboxyfluoresceinand bromodesoxyuridine-labeling experiments showed that lymph node enlargement resulted from modified immigration and enhanced proliferation of lymphocytes, preferentially of B cells. A comparative analysis of B. henselae and the rodent pathogen B. grahamii in wild-type versus interferon-␣/␤-receptor I chaindeficient mice revealed that interferon-␣/␤ is not only differentially induced by these two Bartonella species but also exerts an inhibitory effect on the development of lymphadenopathy both in vitro and in vivo. These data demonstrate that the lymphadenopathy of human CSD can be reproduced and studied in a mouse model and provide the first insights into the underlying immunological mechanisms.

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“…The early production of IFN-b, which also was found to be critical for humoral responses in a mouse infection model (28), may cause production of BAFF by DC populations, further supporting humoral immune responses, by providing signals for classswitch recombination and survival (18,29). Indeed, we observed that DCs secreted BAFF in response to LOS, but only after 72 h, which is well after the initial wave of IFN-b production.…”

Section: Discussionmentioning

confidence: 58%

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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Type I IFN Signaling on Both B and CD4 T Cells Is Required for Protective Antibody Response to Adenovirus

Cited by 53 publications

References 32 publications

Induction of type I interferon by adenovirus-encoded small RNAs

Induction of type I interferon by adenovirus-encoded small RNAs

Lymphadenopathy in a Novel Mouse Model of Bartonella-Induced Cat Scratch Disease Results from Lymphocyte Immigration and Proliferation and Is Regulated by Interferon-α/β

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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