About: Targeted Deletion of FGL2 Leads to Increased Early Viral Replication and Enhanced Adaptive Immunity in a Murine Model of Acute Viral Hepatitis Caused by LCMV WE

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About: Targeted Deletion of FGL2 Leads to Increased Early Viral Replication and Enhanced Adaptive Immunity in a Murine Model of Acute Viral Hepatitis Caused by LCMV WE Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Targeted Deletion of FGL2 Leads to Increased Early Viral Replication and Enhanced Adaptive Immunity in a Murine Model of Acute Viral Hepatitis Caused by LCMV WE
Creator	Levy, Gary Selzner, Nazia Shalev, Itay Zhang, Jianhua Bartczak, Agata Khattar, Ramzi Adeyi, Oyedele Gao, Darrin Luft, Olga Manuel, Justin Shyu, Wendy Urbanellis, Peter Yavorska, Nataliya Phillips, M
Source	Medline; PMC
abstract	Mounting effective innate and adaptive immune responses are critical for viral clearance and the generation of long lasting immunity. It is known that production of inhibitory factors may result in the inability of the host to clear viruses, resulting in chronic viral persistence. Fibrinogen-like protein 2 (FGL2) has been identified as a novel effector molecule of CD4(+)CD25(+) Foxp3(+) regulatory T (Treg) cells that inhibits immune activity by binding to FCγRIIB expressed primarily on antigen presenting cells (APC). In this study, we show that infection of mice with Lymphocytic Choriomeningitis Virus WE (LCMV WE) leads to increased plasma levels of FGL2, which were detected as early as 2 days post-infection (pi) and persisted until day 50 pi. Mice deficient in FGL2 (fgl2(−/−)) had increased viral titers of LCMV WE in the liver early p.i but cleared the virus by day 12 similar to wild type mice. Dendritic cells (DC) isolated from the spleens of LCMV WE infected fgl2(−/−) had increased expression of the DC maturation markers CD80 and MHC Class II compared to wild type (fgl2(+/+)). Frequencies of CD8(+) and CD4(+) T cells producing IFNγ in response to ex vivo peptide re-stimulation isolated from the spleen and lymph nodes were also increased in LCMV WE infected fgl2 (−/−) mice. Increased frequencies of CD8(+) T cells specific for LCMV tetramers GP(33) and NP(396) were detected within the liver of fgl2(−/−) mice. Plasma from fgl2(−/−) mice contained higher titers of total and neutralizing anti-LCMV antibody. Enhanced anti-viral immunity in fgl2(−/−) mice was associated with increased levels of serum alanine transaminase (ALT), hepatic necrosis and inflammation following LCMV WE infection. These data demonstrate that targeting FGL2 leads to early increased viral replication but enhanced anti-viral adaptive T & B cell responses. Targeting FGL2 may enhance the efficacy of current anti-viral therapies for hepatotropic viruses.
has issue date	2013-10-11(xsd:dateTime)
bibo:doi	10.1371/journal.pone.0072309
bibo:pmid	24146739
has license	cc-by
sha1sum (hex)	46ffe37cdfe520a31dadf0a3308b1f7f98d4295d
schema:url	https://doi.org/10.1371/journal.pone.0072309
resource representing a document's title	Targeted Deletion of FGL2 Leads to Increased Early Viral Replication and Enhanced Adaptive Immunity in a Murine Model of Acute Viral Hepatitis Caused by LCMV WE
has PubMed Central identifier	PMC3795679
has PubMed identifier	24146739
schema:publication	PLoS One
resource representing a document's body	covid:46ffe37cdfe520a31dadf0a3308b1f7f98d4295d#body_text
is schema:about of	named entity 'ADAPTIVE IMMUNITY' named entity 'LCMV' named entity 'current' named entity 'protein' named entity 'persisted' named entity 'viral' named entity 'LCMV' named entity 'clearance' named entity 'clear' named entity 'infected' named entity 'therapies' named entity 'LEADS' covid:arg/46ffe37cdfe520a31dadf0a3308b1f7f98d4295d named entity 'IMMUNE ACTIVITY' named entity 'TARGETING' named entity 'HEPATIC NECROSIS' named entity 'ADAPTIVE IMMUNE RESPONSES' named entity 'KNOWN' named entity 'INCREASED EXPRESSION' named entity 'CD25' named entity 'TOTAL' named entity 'CLEAR' named entity 'DATA' named entity 'B CELL' named entity 'CONTAINED' named entity 'LEADS' named entity 'THESE' named entity 'EFFICACY' named entity 'VIRUS' named entity 'CLEARED' named entity 'COMPARED' named entity 'RESPONSE TO' named entity 'RESULT' named entity 'POST' named entity 'DAY' named entity 'MOLECULE' named entity 'ASSOCIATED WITH' named entity 'EFFECTOR' named entity 'VIRAL CLEARANCE' named entity 'CHRONIC' named entity 'ALANINE TRANSAMINASE' named entity 'ISOLATED' named entity 'WILD TYPE' named entity 'HEPATOTROPIC' named entity 'DENDRITIC CELLS' named entity 'SIMILAR' named entity 'INHIBITORY' named entity 'DETECTED' named entity 'VIRAL IMMUNITY' named entity '396' named entity 'MARKERS' named entity 'TARGETED' named entity 'HIGHER' named entity 'INFECTED' named entity 'STIMULATION' named entity 'RESULTING IN' named entity 'DELETION' named entity 'NECROSIS AND INFLAMMATION' named entity 'VIRAL' named entity 'CD4' named entity 'LYMPH NODES' named entity 'LIVER' named entity 'DEFICIENT' named entity 'CRITICAL' named entity 'FGL2' named entity 'FOXP3' named entity 'IMMUNITY' named entity 'CD80'

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