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

Stephen O. Priest, Nicole Baumgarth

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)105-117
Number of pages13
JournalFrontiers in Bioscience - Scholar
Volume5 S
Issue number1
StatePublished - Jan 1 2013

Keywords

  • Antibody
  • B cells
  • B-lymphocytes
  • BALT
  • Bronchus associated lymphoid tissue
  • CD69
  • CD81
  • CD86
  • Cell cycle
  • HA
  • Hemaglutanin
  • Humoral
  • IFN-alpha
  • IFN-beta
  • Ig
  • IgG
  • IgM
  • Immunoglobulin
  • Infection
  • Influenza
  • Innate
  • Isotype
  • Lung
  • Mediastinal lymph node
  • MyD88
  • NLR
  • NOD-like receptor
  • PAMP
  • Pathogen associated molecular pattern
  • PDC
  • Plasmacytoid dendritic cell
  • Respiratory tract
  • Review
  • RIG-I
  • RIG-I like receptor
  • RLR
  • SLE
  • Systemic lupus erythmatosis
  • TLR3
  • TLR7
  • TLR9
  • Toll-like receptor
  • Type-I interferon
  • Virus

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)
  • Medicine(all)

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