Journal
CELL REPORTS
Volume 23, Issue 4, Pages 1085-1098Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.03.097
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Funding
- Australian National Health and Medical Research Council (NHMRC) grants [1037304, 1099262, 1086786]
- CJ Martin Fellowship [613718]
- Iraqi Cultural Attache in Australia
- Queensland Department of Science, Information Technology and Innovation
- Sylvia and Charles Viertel Foundation
- HHMI-Wellcome International Research Scholarship
- Glaxosmithkline
- AITHM
- [1020114]
- National Health and Medical Research Council of Australia [1086786] Funding Source: NHMRC
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Inflammasomes promote immunity to microbial pathogens by regulating the function of IL-1-family cytokines such as IL-18 and IL-1 beta. However, the roles for inflammasomes during parasitic helminth infections remain unclear. We demonstrate that mice and humans infected with gastrointestinal nematodes display increased IL-18 secretion, which in Trichuris-infected or worm antigen-treated mice and in macrophages co-cultured with Trichuris antigens or exosome-like vesicles was dependent on the NLRP3 inflammasome. NLRP3-deficient mice displayed reduced pro-inflammatory type 1 cytokine responses and augmented protective type 2 immunity, which was reversed by IL-18 administration. NLRP3-dependent suppression of immunity partially required CD4(+) cells but was apparent even in Rag1(-/-) mice that lack adaptive immune cells, suggesting that NLRP3 influences both innate and adaptive immunity. These data highlight a role for NLRP3 in limiting protective immunity to helminths, suggesting that targeting the NLRP3 inflammasome may be an approach for limiting the disease burden associated with helminth infections.
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