Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 388-393 |
| Number of pages | 6 |
| Journal | Trends in Parasitology |
| Volume | 27 |
| Issue number | 9 |
| DOIs | |
| State | Published - Sep 2011 |
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ASJC Scopus subject areas
- Infectious Diseases
- Parasitology
Cite this
Innate responses to Toxoplasma gondii in mice and humans. / Pifer, Reed; Yarovinsky, Felix.
In: Trends in Parasitology, Vol. 27, No. 9, 09.2011, p. 388-393.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Innate responses to Toxoplasma gondii in mice and humans
AU - Pifer, Reed
AU - Yarovinsky, Felix
PY - 2011/9
Y1 - 2011/9
N2 - 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.
AB - 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.
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U2 - 10.1016/j.pt.2011.03.009
DO - 10.1016/j.pt.2011.03.009
M3 - Article
C2 - 21550851
AN - SCOPUS:80051765668
VL - 27
SP - 388
EP - 393
JO - Trends in Parasitology
JF - Trends in Parasitology
SN - 1471-4922
IS - 9
ER -