Publications

Detailed Information

An NLRP3 inflammasome–triggered Th2-biased adaptive immune response promotes leishmaniasis : An NLRP3 inflammasome-triggered Th2-biased adaptive immune response promotes leishmaniasis

DC Field Value Language
dc.contributor.authorGurung, Prajwal-
dc.contributor.authorKarki, Rajendra-
dc.contributor.authorVogel, Peter-
dc.contributor.authorWatanabe, Makiko-
dc.contributor.authorBix, Mark-
dc.contributor.authorLamkanfi, Mohamed-
dc.contributor.authorKanneganti, Thirumala-Devi-
dc.date.accessioned2024-05-16T01:59:35Z-
dc.date.available2024-05-16T01:59:35Z-
dc.date.created2023-05-08-
dc.date.created2023-05-08-
dc.date.created2023-05-08-
dc.date.issued2015-03-
dc.identifier.citationJournal of Clinical Investigation, Vol.125 No.3, pp.1329-1338-
dc.identifier.issn0021-9738-
dc.identifier.urihttps://hdl.handle.net/10371/203061-
dc.description.abstractLeishmaniasis is a major tropical disease that can present with cutaneous, mucocutaneous, or visceral manifestation and affects millions of individuals, causing substantial morbidity and mortality in-third-world countries. The development of a Th1-adaptive immune response is associated with resistance to developing Leishmania major (L. major) infection. Inflammasomes are key components of the innate immune system that contribute to host defense against bacterial and viral pathogens; however, their role in regulating adaptive immunity during infection with protozoan parasites is less studied. Here, we demonstrated that the NLRP3 inflammasome balances Th1/Th2 responses during leishmaniasis. Mice lacking the inflammasome components NLRP3, ASC, or caspase 1 on a Leishmania-susceptible BALB/c background exhibited defective IL-1 beta and IL-18 production at the infection site and were resistant to cutaneous L. major infection. Moreover, we determined that production of IL-18 propagates disease in susceptible BALB/c mice by promoting the Th2 cytokine IL-4, and neutralization of IL-18 in these animals reduced L. major titers and footpad swelling. In conclusion, our results indicate that activation of the NLRP3 inflammasome is detrimental during leishmaniasis and suggest that IL-18 neutralization has potential as a therapeutic strategy to treat leishmaniasis patients.-
dc.language영어-
dc.publisherAmerican Society for Clinical Investigation-
dc.titleAn NLRP3 inflammasome–triggered Th2-biased adaptive immune response promotes leishmaniasis-
dc.title.alternativeAn NLRP3 inflammasome-triggered Th2-biased adaptive immune response promotes leishmaniasis-
dc.typeArticle-
dc.identifier.doi10.1172/JCI79526-
dc.citation.journaltitleJournal of Clinical Investigation-
dc.identifier.wosid000350616500043-
dc.identifier.scopusid2-s2.0-84924087828-
dc.citation.endpage1338-
dc.citation.number3-
dc.citation.startpage1329-
dc.citation.volume125-
dc.description.isOpenAccessY-
dc.contributor.affiliatedAuthorKarki, Rajendra-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusFACTOR TNF-ALPHA-
dc.subject.keywordPlusCUTANEOUS LEISHMANIASIS-
dc.subject.keywordPlusT-CELLS-
dc.subject.keywordPlusINTERFERON-GAMMA-
dc.subject.keywordPlusNITRIC-OXIDE-
dc.subject.keywordPlusIFN-GAMMA-
dc.subject.keywordPlusMURINE LEISHMANIASIS-
dc.subject.keywordPlusHOST-DEFENSE-
dc.subject.keywordPlusINBRED MICE-
dc.subject.keywordPlusBALB/C MICE-
Appears in Collections:
Files in This Item:
There are no files associated with this item.

Related Researcher

  • College of Natural Sciences
  • School of Biological Sciences
Research Area Cytokine Storm, Host Defense, Innate Immunity in Metabolic and Inflammatory Diseases

Altmetrics

Item View & Download Count

  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Share