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- Title
IL-33 promotes innate lymphoid celldependent IFN-g production required for innate immunity to Toxoplasma gondii.
- Authors
Clark, Joseph T.; Christian, David A.; Gullicksrud, Jodi A.; Perry, Joseph A.; Park, Jeongho; Jacquet, Maxime; Tarrant, James C.; Radaelli, Enrico; Silver, Jonathan; Hunter, Christopher A.
- Abstract
IL-33 is an alarmin required for resistance to the parasite Toxoplasma gondii, but its role in innate resistance to this organism is unclear. Infection with T. gondii promotes increased stromal cell expression of IL-33, and levels of parasite replication correlate with release of IL-33 in affected tissues. In response to infection, a subset of innate lymphoid cells (ILC) emerges composed of IL-33R+ NK cells and ILC1s. In Rag1/mice, where NK cells and ILC1 production of IFN-g mediate innate resistance to T. gondii, the loss of the IL-33R resulted in reduced ILC responses and increased parasite replication. Furthermore, administration of IL-33 to Rag1-/- mice resulted in a marked decrease in parasite burden, increased production of IFN-g, and the recruitment and expansion of inflammatory monocytes associated with parasite control. These protective effects of exogenous IL-33 were dependent on endogenous IL-12p40 and the ability of IL-33 to enhance ILC production of IFN-g. These results highlight that IL-33 synergizes with IL-12 to promote ILC-mediated resistance to T. gondii.
- Subjects
INTERLEUKIN-33; NATURAL immunity; KILLER cells; INNATE lymphoid cells; PARASITES; TOXOPLASMA gondii; STROMAL cells
- Publication
eLife, 2021, p1
- ISSN
2050-084X
- Publication type
Article
- DOI
10.7554/eLife.65614