Influenza Virus Infection Causes Global Respiratory Tract B Cell Response Modulation via Innate Immune Signals

Chang, W. L. William; Coro, Elizabeth S.; Rau, Friederike C.; Xiao, Yuanyuan; Erle, David J.; Baumgarth, Nicole

doi:10.4049/jimmunol.178.3.1457

Cited by 61 publications

(77 citation statements)

References 49 publications

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“…Previous reports demonstrated that type I IFN mediates activation of LN-resident B cells in response to influenza or West Nile virus infection (48)(49)(50)(51). In the context of West Nile virus infection, the authors excluded macrophages as type I IFN-producing cells, but the actual cellular source was not identified for either infection model.…”

Section: Discussionmentioning

confidence: 89%

Plasmacytoid dendritic cells promote rotavirus-induced human and murine B cell responses

Deal

Lahl²,

Narváez³

et al. 2013

J. Clin. Invest.

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B cell-dependent immunity to rotavirus, an important intestinal pathogen, plays a significant role in viral clearance and protects against reinfection. Human in vitro and murine in vivo models of rotavirus infection were used to delineate the role of primary plasmacytoid DCs (pDCs) in initiating B cell responses. Human pDCs were necessary and sufficient for B cell activation induced by rotavirus. Type I IFN recognition by B cells was essential for rotavirus-mediated B cell activation in vitro and murine pDCs and IFN-α/β-mediated B cell activation after in vivo intestinal rotavirus infection. Furthermore, rotavirus-specific serum and mucosal antibody responses were defective in mice lacking functional pDCs at the time of infection. These data demonstrate that optimal B cell activation and virus-specific antibody secretion following mucosal infection were a direct result of pDC-derived type I IFN. Importantly, viral shedding significantly increased in pDC-deficient mice, suggesting that pDC-dependent antibody production influences viral clearance. Thus, mucosal pDCs critically influence the course of rotavirus infection through rotavirus recognition and subsequent IFN production and display powerful adjuvant properties to initiate and enhance humoral immunity.

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Section: Discussionmentioning

confidence: 89%

Plasmacytoid dendritic cells promote rotavirus-induced human and murine B cell responses

Deal

Lahl²,

Narváez³

et al. 2013

J. Clin. Invest.

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“…At this time, we cannot exclude other mechanisms that may also contribute to the enhanced Ab response in G9KO mice. For instance Gal-9 deficiency may limit other mechanisms of suppression (25), resulting in increased levels of factors that act directly on B cells to promote their activation (26).…”

Section: Discussionmentioning

confidence: 99%

T cell immunoglobulin and mucin protein-3 (Tim-3)/Galectin-9 interaction regulates influenza A virus-specific humoral and CD8 T-cell responses

Sharma

Sundararajan

Suryawanshi

et al. 2011

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

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Reactions to pathogens are usually tuned to effect immunity and limit tissue damage. Several host counterinflammatory mechanisms inhibit tissue damage but these may also act to constrain the effectiveness of immunity to acute infections, as we demonstrate in mice acutely infected with influenza A virus (IAV). We show that compared with wild type (WT), galectin-9 knockout (G9KO) mice mounted a more robust acute phase virus-specific CD8 T-cell response as well as higher and more rapid virus-specific serum IgM, IgG, and IgA responses and also cleared virus more rapidly than did WT mice. Blocking galectin-9 signals to Tim-3-expressing cells using a Tim-3 fusion protein resulted in improved immune responses in WT mice. When IAV immune mice were challenged with a heterologous IAV, the secondary IAV-specific CD8 T-cell responses were fourto fivefold higher in G9KO compared with WT mice. Our results indicate that manipulating galectin signals may represent a convenient approach to improve immune responses to some vaccines.T he host immune response to pathogens needs precise regulation to minimize tissue damage while still achieving defense (1, 2). Some bystander tissue damage usually happens because several host defenses can destroy cells or orchestrate inflammatory reactions. With chronic infections, for example, immune-mediated tissue damage would be more severe were it not for several cellular and chemical host components that inhibit inflammatory reactions (1). However, the activity of some of these counterinflammatory mechanisms could act to constrain the efficiency of protective immune components (3). For instance, regulatory T cells (Tregs) can inhibit inflammatory reactions associated with chronic virus infections (4), but the same Treg response can also limit the magnitude of protective immunity to a virus or induced by a vaccine (5, 6). Other host components may also function to limit and help resolve inflammatory reactions. These include some cytokines (7), groups of molecules derived from omega-3 polyunsaturated fatty acids (8), as well as some of the carbohydrate binding proteins of the galectin family (9). Galectin-9 (Gal-9), for example, upon binding to Tim-3 on T cells acts to limit the extent of immunopathological lesions in autoimmunity (10) as well as in some chronic infections (11-13). In the present study, we investigated whether the inhibitory effects of Gal-9 on Tim-3-expressing cells could influence the outcome of acute infection with influenza A virus (IAV). We demonstrate that animals lacking the regulatory effects of Gal-9/Tim-3 triggering mounted superior CD8 T-cell and humoral immune responses and they were more refractory to IAV. Moreover, IAV immune G9KO mice challenged with a heterologous IAV strain generated better virus-specific memory CD8 T-cell responses than WT animals. Our results indicate that manipulating galectin signaling may represent a convenient approach to improve responses to some vaccines. Results Virus-Specific CD8 T cells Up-Regulate Tim-3 Expression after IAVInfection. ...

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“…Rotavirus infection promoted substantial T-cell-independent B-cell activation by day 3 in the mesenteric lymph nodes (LN) in wild-type mice (6,7). Polyclonal B-cell activation and virus-specific antibody responses against influenza virus were dependent on type I interferon (IFN) signaling (11,13). In contrast, B-cell activation of mediastinal LN after murine gammaherpesvirus 68 infection was delayed until day 10 and required T-cell help (52).…”

mentioning

confidence: 99%

Early B-Cell Activation after West Nile Virus Infection Requires Alpha/Beta Interferon but Not Antigen Receptor Signaling

Purtha¹,

Chachu²,

Virgin³

et al. 2008

J Virol

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Influenza Virus Infection Causes Global Respiratory Tract B Cell Response Modulation via Innate Immune Signals

Cited by 61 publications

References 49 publications

Plasmacytoid dendritic cells promote rotavirus-induced human and murine B cell responses

Plasmacytoid dendritic cells promote rotavirus-induced human and murine B cell responses

T cell immunoglobulin and mucin protein-3 (Tim-3)/Galectin-9 interaction regulates influenza A virus-specific humoral and CD8 T-cell responses

Early B-Cell Activation after West Nile Virus Infection Requires Alpha/Beta Interferon but Not Antigen Receptor Signaling

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