| First Author | Alhallaf R | Year | 2018 |
| Journal | Cell Rep | Volume | 23 |
| Issue | 4 | Pages | 1085-1098 |
| PubMed ID | 29694887 | Mgi Jnum | J:270898 |
| Mgi Id | MGI:6278339 | Doi | 10.1016/j.celrep.2018.03.097 |
| Citation | Alhallaf R, et al. (2018) The NLRP3 Inflammasome Suppresses Protective Immunity to Gastrointestinal Helminth Infection. Cell Rep 23(4):1085-1098 |
| abstractText | Inflammasomes promote immunity to microbial pathogens by regulating the function of IL-1-family cytokines such as IL-18 and IL-1beta. 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. |
