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dc.contributor.authorHe, Xing
dc.contributor.authorXie, Jun
dc.contributor.authorWang, Yange
dc.contributor.authorFan, Xiaobin
dc.contributor.authorSu, Qin
dc.contributor.authorSun, Yue
dc.contributor.authorLei, Nanhang
dc.contributor.authorZhang, Dongmei
dc.contributor.authorGao, Guangping
dc.contributor.authorPan, Weiqing
dc.date2022-08-11T08:09:50.000
dc.date.accessioned2022-08-23T16:45:06Z
dc.date.available2022-08-23T16:45:06Z
dc.date.issued2018-03-19
dc.date.submitted2018-05-30
dc.identifier.citation<p>PLoS Pathog. 2018 Mar 19;14(3):e1006957. doi: 10.1371/journal.ppat.1006957. eCollection 2018 Mar. <a href="https://doi.org/10.1371/journal.ppat.1006957">Link to article on publisher's site</a></p>
dc.identifier.issn1553-7366 (Linking)
dc.identifier.doi10.1371/journal.ppat.1006957
dc.identifier.pmid29554131
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40620
dc.description.abstractThe type 2 immune response is the central mechanism of disease progression in schistosomiasis, but the signals that induce it after infection remain elusive. Aberrant microRNA (miRNA) expression is a hallmark of human diseases including schistosomiasis, and targeting the deregulated miRNA can mitigate disease outcomes. Here, we demonstrate that efficient and sustained elevation of miR-203-3p in liver tissues, using the highly hepatotropic recombinant adeno-associated virus serotype 8 (rAAV8), protects mice against lethal schistosome infection by alleviating hepatic fibrosis. We show that miR-203-3p targets interleukin-33 (IL-33), an inducer of type 2 immunity, in hepatic stellate cells to regulate the expansion and IL-13 production of hepatic group 2 innate lymphoid cells during infection. Our study highlights the potential of rAAV8-mediated miR-203-3p elevation as a therapeutic intervention for fibrotic diseases.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=29554131&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright: © 2018 He et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectFibrosis
dc.subjectMicroRNAs
dc.subjectParasitic diseases
dc.subjectCollagens
dc.subjectSchistosomiasis
dc.subjectMouse models
dc.subjectLiver fibrosis
dc.subjectSchistosoma
dc.subjectImmunity
dc.subjectImmunology of Infectious Disease
dc.subjectParasitic Diseases
dc.subjectParasitology
dc.subjectTherapeutics
dc.titleDown-regulation of microRNA-203-3p initiates type 2 pathology during schistosome infection via elevation of interleukin-33
dc.typeJournal Article
dc.source.journaltitlePLoS pathogens
dc.source.volume14
dc.source.issue3
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4434&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3423
dc.identifier.contextkey12222315
refterms.dateFOA2022-08-23T16:45:07Z
html.description.abstract<p>The type 2 immune response is the central mechanism of disease progression in schistosomiasis, but the signals that induce it after infection remain elusive. Aberrant microRNA (miRNA) expression is a hallmark of human diseases including schistosomiasis, and targeting the deregulated miRNA can mitigate disease outcomes. Here, we demonstrate that efficient and sustained elevation of miR-203-3p in liver tissues, using the highly hepatotropic recombinant adeno-associated virus serotype 8 (rAAV8), protects mice against lethal schistosome infection by alleviating hepatic fibrosis. We show that miR-203-3p targets interleukin-33 (IL-33), an inducer of type 2 immunity, in hepatic stellate cells to regulate the expansion and IL-13 production of hepatic group 2 innate lymphoid cells during infection. Our study highlights the potential of rAAV8-mediated miR-203-3p elevation as a therapeutic intervention for fibrotic diseases.</p>
dc.identifier.submissionpathoapubs/3423
dc.contributor.departmentDepartment of Microbiology and Physiological Systems
dc.contributor.departmentHorae Gene Therapy Center
dc.source.pagese1006957


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Copyright: © 2018 He et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Except where otherwise noted, this item's license is described as Copyright: © 2018 He et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.