Gut Commensal Bacteria Direct a Protective Immune Response against Toxoplasma gondii

Alicia Benson, Reed Pifer, Cassie L. Behrendt, Lora V. Hooper, Felix Yarovinsky

Research output: Contribution to journalArticlepeer-review

167 Scopus citations


Toxoplasma gondii is a universally distributed pathogen that infects over one billion people worldwide. Host resistance to this protozoan parasite depends on a Th1 immune response with potent production of the cytokines interleukin-12 and interferon γ. Although Toll-like receptor 11 (TLR11) plays a major role in controlling Th1 immunity to this pathogen in mice, this innate immune receptor is nonfunctional in humans, and the mechanisms of TLR11-independent sensing of T. gondii remain elusive. Here, we show that oral infection by T. gondii triggers a TLR11-independent but MyD88-dependent Th1 response that is impaired in TLR2xTLR4 double knockout and TLR9 single knockout mice. These mucosal innate and adaptive immune responses to T. gondii rely on the indirect stimulation of dendritic cells by normal gut microflora. Thus, our results reveal that gut commensal bacteria can serve as molecular adjuvants during parasitic infection, providing indirect immunostimulation that protects against T. gondii in the absence of TLR11.

Original languageEnglish (US)
Pages (from-to)187-196
Number of pages10
JournalCell Host and Microbe
Issue number2
StatePublished - Aug 20 2009



ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Virology


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