| First Author | Zaiss MM | Year | 2013 |
| Journal | PLoS Pathog | Volume | 9 |
| Issue | 8 | Pages | e1003531 |
| PubMed ID | 23935505 | Mgi Jnum | J:214162 |
| Mgi Id | MGI:5588514 | Doi | 10.1371/journal.ppat.1003531 |
| Citation | Zaiss MM, et al. (2013) IL-1beta suppresses innate IL-25 and IL-33 production and maintains helminth chronicity. PLoS Pathog 9(8):e1003531 |
| abstractText | Approximately 2 billion people currently suffer from intestinal helminth infections, which are typically chronic in nature and result in growth retardation, vitamin A deficiency, anemia and poor cognitive function. Such chronicity results from co-evolution between helminths and their mammalian hosts; however, the molecular mechanisms by which these organisms avert immune rejection are not clear. We have found that the natural murine helminth, Heligmosomoides polygyrus bakeri (Hp) elicits the secretion of IL-1beta in vivo and in vitro and that this cytokine is critical for shaping a mucosal environment suited to helminth chronicity. Indeed in mice deficient for IL-1beta (IL-1beta(-/-)), or treated with the soluble IL-1betaR antagonist, Anakinra, helminth infection results in enhanced type 2 immunity and accelerated parasite expulsion. IL-1beta acts to decrease production of IL-25 and IL-33 at early time points following infection and parasite rejection was determined to require IL-25. Taken together, these data indicate that Hp promotes the release of host-derived IL-1beta that suppresses the release of innate cytokines, resulting in suboptimal type 2 immunity and allowing pathogen chronicity. |
