About: Recovery from Mouse Hepatitis Virus Infection Depends on Recruitment of CD8+ Cells Rather Than Activation of Intrahepatic CD4+αβ−TCRinter or NK-T Cells

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: Recovery from Mouse Hepatitis Virus Infection Depends on Recruitment of CD8+ Cells Rather Than Activation of Intrahepatic CD4+αβ−TCRinter or NK-T Cells 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	Recovery from Mouse Hepatitis Virus Infection Depends on Recruitment of CD8+ Cells Rather Than Activation of Intrahepatic CD4+αβ−TCRinter or NK-T Cells
Creator	Lamontagne, Lucie Lusignan, Suzanne Page, Christian
Source	Elsevier; Medline; PMC
abstract	Abstract Mouse hepatitis virus (MHV) provides an excellent animal model for the study of the immunopathological mechanisms involved in hepatic viral diseases. We previously generated an attenuated viral variant, YAC-MHV3, which induces a subclinical disease and recovery within 15 days. In contrast, the L2-MHV3 strain induces the development of a fulminant hepatitis, leading to death within 3 days. In this paper, we document intrahepatic and splenic T cell subpopulations involved in the hepatitis process and viral elimination identified in attenuated or pathogenic MHV3-infected C57BL/6 mice. Percentages of intrahepatic CD4+ cells decreased in attenuated YAC-MHV3-infected mice, while they increased in mice infected with pathogenic L2-MHV3, compared with uninfected animals. Moreover, in YAC-MHV3-infected mice, the percentages of intrahepatic CD8+ cells slightly decreased at 24 h pi, then increased until 15 days pi. In contrast, the CD4/CD8 ratios of splenic lymphoid subpopulations increased in the first days of infection and returned to normal values at 15 days pi. Intrahepatic NK1.1+αβ − TCRinter cells decreased in both virally infected groups of mice, while CD4+αβ − TCRinter LFA-1high cells increased in L2-MHV3-infected mice, in contrast with what was seen in YAC-MHV3-infected mice. However, these cells became anergic following Con A or PHA stimulation. Ex vivo studies showed that only the intrahepatic CD8+ cells that were increased in YAC-MHV3-infected mice could be stimulated by lectins. In addition, in vitro viral infections revealed that L2-MHV3 viral infection led to an increase of intrahepatic CD4+αβ − TCRinter cells in the absence of CD8+ cells only. These results indicate that the attenuated phenotype of the YAC-MHV3 virus is related to two different mechanisms: the first involves no increase of intrahepatic CD4+αβ − TCRinter or NK-T cells, while the second favors the recruitment and activation of CD8+ cells in liver. The results are discussed in relation to the integrity of intrahepatic immune tolerance mechanisms and immune-mediated viral elimination.
has issue date	2001-12-31(xsd:dateTime)
bibo:doi	10.1006/clim.2001.5131
bibo:pmid	11726227
has license	els-covid
sha1sum (hex)	78924545c40b6498e80f955b1496df19d1e4a324
schema:url	https://doi.org/10.1006/clim.2001.5131
resource representing a document's title	Recovery from Mouse Hepatitis Virus Infection Depends on Recruitment of CD8+ Cells Rather Than Activation of Intrahepatic CD4+αβ−TCRinter or NK-T Cells
has PubMed Central identifier	PMC7128857
has PubMed identifier	11726227
schema:publication	Clinical Immunology
resource representing a document's body	covid:78924545c40b6498e80f955b1496df19d1e4a324#body_text
is schema:about of	named entity 'animal model' named entity 'mice' named entity 'elimination' named entity 'disease' named entity 'Infection' named entity 'Cells' covid:arg/78924545c40b6498e80f955b1496df19d1e4a324 named entity 'mice' named entity 'MHV' named entity 'subclinical' named entity 'CD8' named entity 'CD4' named entity 'animal model' named entity 'CD8' named entity 'viral diseases' named entity 'hepatic' named entity 'strain' named entity 'formaldehyde' named entity 'CD4' named entity 'CD11a' named entity 'lymphoid cells' named entity 'PHA' named entity 'lymphocytes' named entity 'liver' named entity 'CD4' named entity 'liver' named entity 'C57BL/6' named entity 'subclinical infection' named entity 'lymphocytes' named entity 'vascular disorders' named entity 'leukocyte' named entity 'hepatotropic' named entity 'centrifuged' named entity 'venous blood' named entity 'Mouse hepatitis virus' named entity 'antibodies' named entity 'lymphoid cells' named entity 'CD4' named entity 'down-regulation' named entity 'C57BL/6' named entity 'mice' named entity 'mice' named entity 'cytokines' named entity 'phenotype' named entity 'mononuclear cells' named entity 'surface markers' named entity 'CD4' named entity 'macrophages' named entity 'PBS' named entity 'mice' named entity 'lymphoid cells' named entity 'CD8' named entity 'microtiter plates' named entity 'B220' named entity 'viral infection' named entity 'viral replication' named entity 'PBS' named entity 'tolerance mechanisms' named entity 'spleen' named entity 'CD8' named entity 'mononuclear cells' named entity 'mice' named entity 'CD4' named entity 'lectins' named entity 'infection' named entity 'mice' named entity 'CD4' named entity 'CD4' named entity 'antibodies' named entity 'lymphoid organs' named entity 'hepatitis' named entity 'antibodies' named entity 'PBS' named entity 'CD8' named entity 'viral replication' named entity 'immune response' named entity 'viral infection' named entity 'immune-mediated' named entity 'IL-4'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2024 OpenLink Software