Innate responses to Toxoplasma gondii in mice and humans

Trends Parasitol. 2011 Sep;27(9):388-93. doi: 10.1016/


Primary infection with Toxoplasma gondii stimulates production of high levels of interleukin 12 (IL-12) and interferon γ (IFN-γ) by cells of the innate immune system. These two cytokines are central to resistance to T. gondii. Signaling through the Toll-like receptor (TLR) adaptor protein MyD88 is indispensible for activating early innate immune responses. Recent studies have established that TLR11 plays a dominant role in sensing T. gondii. At the same time, TLR11 is represented in humans only by a pseudogene, and the major question of how innate and adaptive immune responses occur in the absence of TLR11 remains unanswered. In this article, similarities and differences in sensors and effector molecules that determine host resistance to the parasite in humans and mice are discussed.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adaptive Immunity
  • Animals
  • Bacteria / immunology
  • Host-Pathogen Interactions*
  • Humans
  • Immunity, Innate*
  • Immunity, Mucosal
  • Interferon-gamma / immunology
  • Interleukin-12 / immunology
  • Intestines / immunology
  • Intestines / microbiology
  • Intestines / parasitology
  • Mice
  • Myeloid Differentiation Factor 88 / immunology
  • Signal Transduction
  • Species Specificity
  • Toll-Like Receptors / immunology
  • Toxoplasma / immunology*
  • Toxoplasma / pathogenicity
  • Toxoplasmosis / immunology*
  • Toxoplasmosis / parasitology


  • MYD88 protein, human
  • Myd88 protein, mouse
  • Myeloid Differentiation Factor 88
  • TLR11 protein, human
  • Tlr11 protein, mouse
  • Toll-Like Receptors
  • Interleukin-12
  • Interferon-gamma