Reduced severity of peanut-induced anaphylaxis in TLR9-deficient mice is associated with selective defects in humoral immunity

M. C. Berin*, W. Wang

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

Signaling through the innate immune system can promote or suppress allergic sensitization. Toll-like receptor 9 (TLR9) has modulatory effects on the mucosal immune system, and we hypothesized that TLR9 would influence susceptibility to allergic sensitization to foods. We observed that TLR9-/- mice were resistant to peanut-induced anaphylaxis. This was associated with a significant impairment in total immunoglobulin E (IgE) and peanut-specific IgE and IgA, but not IgG1 or Th2 cytokine production. TLR9-/- mice had reduced development of Peyer's patches, but resistance to sensitization was not restricted to oral routes. Rag1-deficient mice were reconstituted with TLR9+/+ or -/- B cells plus CD4+ T cells. TLR9-/- B cells regained the ability to produce IgE in the presence of a wild-type environment. Our results demonstrate that TLR9 on an unknown cell type is required for the development of IgE-producing B cells, and we conclude that TLR9 signaling indirectly shapes the immune response for optimal IgE production.

Original languageEnglish (US)
Pages (from-to)114-121
Number of pages8
JournalMucosal Immunology
Volume6
Issue number1
DOIs
StatePublished - Jan 2013

Funding

This work was funded by U19AI66738 and U19AI044236 (from NIAID) and R834064 (from EPA). We thank the CoFAR basic science group (Kim Bottomly, Michael Caplan, Pierre Pochard, and Brian Vickery) as well as Hugh Sampson and Lloyd Mayer for helpful discussions.

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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