[Frontiers in Bioscience S5, 105-117, January 1, 2013]

The role of innate signals in B cell immunity to influenza virus

Stephen O. Priest1, Nicole Baumgarth1

1Graduate Group in Immunology and Center for Comparative Medicine, University of California, Davis, Davis, CA 95616, USA


1. Abstract
2. Introduction
3. Primary B cell responses to influenza virus infection
4. Innate signal-regulated B cell responses to influenza
4.1. Pattern recognition receptors triggered by influenza infection
4.2. TLR-mediated regulation of conventional antiviral B cell responses
4.3. Innate signals regulate B-1 cell responses to influenza
4.4.Type I IFN-mediated regulation of conventional antiviral B cell responses
4.4.1. Immune-enhancing effects of type-I IFN on B cells
4.4.2. IFNa/b regulate TLR-signaling by B cells
4.4.3. Immune-suppressive effects of type-I IFN on B cells
5. Conclusions
6. Acknowledgements
7. References


Decades of research on mammalian immunity to influenza virus infection have thoroughly established the important contributions made by both the innate and adaptive responses in containing the infection, and in eliminating the virus and protecting from reinfection, respectively. While rapid non-specific innate response is functionally distinct from, yet elegantly complementary to, the delayed-but-specific adaptive response, an increasing number of studies have provided evidence suggesting signals generated during the early innate response can have a significant impact on the quality of the later adaptive response, particularly in the context of influenza virus infection. From these findings emerged the notion that certain innate signals can act directly on B cells, and that this can even help activate virus specific B cells independent of T cell help, marking a major shift away from the current two-signal paradigm of lymphocyte activation. Here we review the current understanding of early B cell responses to influenza virus infection and the role of innate signals (particularly IFN-I and TLR7) in shaping this response.