About: Deletion of Fibrinogen-like Protein 2 (FGL-2), a Novel CD4(+) CD25(+) Treg Effector Molecule, Leads to Improved Control of Echinococcus multilocularis Infection in Mice

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About: Deletion of Fibrinogen-like Protein 2 (FGL-2), a Novel CD4(+) CD25(+) Treg Effector Molecule, Leads to Improved Control of Echinococcus multilocularis Infection in Mice Goto Sponge NotDistinct Permalink

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Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Deletion of Fibrinogen-like Protein 2 (FGL-2), a Novel CD4(+) CD25(+) Treg Effector Molecule, Leads to Improved Control of Echinococcus multilocularis Infection in Mice
Creator	Gottstein, Bruno Müller, Norbert Levy, Gary Shalev, Itay Wen, Hao Hemphill, Andrew Blagosklonov, Oleg Grandgirard, Denis Lin, Renyong Lu, Xiaomei Spiliotis, Markus Wang, Junhua Leib, Stephen Vuitton, Dominique
Source	PMC
abstract	BACKGROUND: The growth potential of the tumor-like Echinococcus multilocularis metacestode (causing alveolar echinococcosis, AE) is directly linked to the nature/function of the periparasitic host immune-mediated processes. We previously showed that Fibrinogen-like-protein 2 (FGL2), a novel CD4(+)CD25(+) Treg effector molecule, was over-expressed in the liver of mice experimentally infected with E. multilocularis. However, little is known about its contribution to the control of this chronic helminth infection. METHODS/FINDINGS: Key parameters for infection outcome in E. multilocularis-infected fgl2(-/-) (AE-fgl2(-/-)) and wild type (AE-WT) mice at 1 and 4 month(s) post-infection were (i) parasite load (i. e. wet weight of parasitic metacestode tissue), and (ii) parasite cell proliferation as assessed by determining E. multilocularis 14-3-3 gene expression levels. Serum FGL2 levels were measured by ELISA. Spleen cells cultured with ConA for 48h or with E. multilocularis Vesicle Fluid (VF) for 96h were analyzed ex-vivo and in-vitro. In addition, spleen cells from non-infected WT mice were cultured with rFGL2/anti-FGL2 or rIL-17A/anti-IL-17A for further functional studies. For Treg-immune-suppression-assays, purified CD4(+)CD25(+) Treg suspensions were incubated with CD4(+) effector T cells in the presence of ConA and irradiated spleen cells as APCs. Flow cytometry and qRT-PCR were used to assess Treg, Th17-, Th1-, Th2-type immune responses and maturation of dendritic cells. We showed that AE-fgl2(-/-) mice exhibited (as compared to AE-WT-animals) (a) a significantly lower parasite load with reduced proliferation activity, (b) an increased T cell proliferative response to ConA, (c) reduced Treg numbers and function, and (d) a persistent capacity of Th1 polarization and DC maturation. CONCLUSIONS: FGL2 appears as one of the key players in immune regulatory processes favoring metacestode survival by promoting Treg cell activity and IL-17A production that contributes to FGL2-regulation. Prospectively, targeting FGL2 could be an option to develop an immunotherapy against AE and other chronic parasitic diseases.
has issue date	2015-05-08(xsd:dateTime)
bibo:doi	10.1371/journal.pntd.0003755
bibo:pmid	25955764
has license	cc-by
sha1sum (hex)	7bab005205a7ee772e476d7dbcf5eee3aed12826
schema:url	https://doi.org/10.1371/journal.pntd.0003755
resource representing a document's title	Deletion of Fibrinogen-like Protein 2 (FGL-2), a Novel CD4(+) CD25(+) Treg Effector Molecule, Leads to Improved Control of Echinococcus multilocularis Infection in Mice
has PubMed Central identifier	PMC4425495
has PubMed identifier	25955764
schema:publication	PLoS Negl Trop Dis
resource representing a document's body	covid:7bab005205a7ee772e476d7dbcf5eee3aed12826#body_text
is schema:about of	named entity 'alveolar echinococcosis' named entity 'The' named entity 'host' named entity 'Protein' named entity 'CD25' named entity 'Novel' covid:arg/7bab005205a7ee772e476d7dbcf5eee3aed12826 named entity 'mice' named entity 'immune-mediated' named entity 'CD25' named entity 'potential' named entity 'Echinococcus' named entity 'helminth infection' named entity 'immune response' named entity 'pro-inflammatory cytokines' named entity 'Negative control' named entity 'parasite' named entity 'dendritic cell' named entity 'CD8 +' named entity 'E. multilocularis' named entity 'fibrinogen' named entity 'IL-17A' named entity 'DCs' named entity 'one-way ANOVA' named entity 'E. multilocularis' named entity 'IL-17A' named entity 'infection' named entity 'IFN-γ' named entity 'immune tolerance' named entity 'E. multilocularis' named entity 'infection' named entity 'Th2' named entity 'Tregs' named entity 'gene' named entity 'Germany' named entity 'intracellular' named entity 'down-regulate' named entity 'DCs' named entity 'E. multilocularis' named entity 'mRNA' named entity 'E. multilocularis' named entity 'staining' named entity 'monoclonal antibodies' named entity 'RNA' named entity 'Th1' named entity 'CD4 +' named entity 'CD11b' named entity 'CD8 +' named entity 'cytokine' named entity 'knock-out mice' named entity 'Tregs' named entity 'one-way ANOVA' named entity 'San Diego' named entity 'housekeeping gene' named entity 'CD11b' named entity 'Switzerland' named entity 'infection' named entity 'E. multilocularis' named entity 'IL-17A' named entity '14-3-3' named entity 'CD86' named entity 'Miltenyi Biotec' named entity 'intraperitoneally' named entity 'IL-17A' named entity 'cell proliferation' named entity 'cell functions' named entity 'serum' named entity 'DCs'

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