About: α4-integrins control viral meningoencephalitis through differential recruitment of T helper cell subsets

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About: α4-integrins control viral meningoencephalitis through differential recruitment of T helper cell subsets 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
title	α4-integrins control viral meningoencephalitis through differential recruitment of T helper cell subsets
Creator	Drexler, Ingo Hemmer, Bernhard Gasteiger, Georg Heikenwälder, Mathias Heink, Sylvia Korn, Thomas Muschaweckh, Andreas Petermann, Franziska Rothhammer, Veit Busch, Dirk
source	Medline; PMC
abstract	INTRODUCTION: Natalizumab blocks α4-integrins and is a prototypic agent for a series of anti-inflammatory drugs that impair trafficking of immune cells into the CNS. However, modulation of the access of immune cells to the CNS is associated with impaired immune surveillance and detrimental viral infections of the CNS. Here, we explored the potency of cellular immune responses within the CNS to protect against viral encephalitis in mice with T cell conditional disruption of VLA-4 integrin (α4β1) expression. RESULTS: While VLA-4 expression in virus specific Th1 cells is non-redundant for their ability to access the CNS, α4-integrin deficient Th17 cells enter the CNS compartment and generate an inflammatory milieu upon intrathecal vaccinia virus (VV) infection. However, in contrast to Th1 cells that can adopt direct cytotoxic properties, Th17 cells fail to clear the virus due to insufficient Eomes induced perforin-1 expression. CONCLUSION: The quality of the intrathecal cellular antiviral response under conditions of impaired VLA-4 function jeopardizes host protection. Our functional in vivo data extend our mechanistic understanding of anti-viral immunity in the CNS and help to estimate the risk potential of upcoming therapeutic agents that target the trafficking of immune cells into distinct anatomical compartments.
has issue date	2014-03-07(xsd:dateTime)
bibo:doi	10.1186/2051-5960-2-27
bibo:pmid	24606807
has license	cc-by
sha1sum (hex)	ab8da309a4060c4f4a3774c3ec9e7ebdc5a3a74e
schema:url	https://doi.org/10.1186/2051-5960-2-27
resource representing a document's title	α4-integrins control viral meningoencephalitis through differential recruitment of T helper cell subsets
has PubMed Central identifier	PMC4029267
has PubMed identifier	24606807
schema:publication	Acta Neuropathol Commun
resource representing a document's body	covid:ab8da309a4060c4f4a3774c3ec9e7ebdc5a3a74e#body_text
is schema:about of	named entity 'intrathecal' named entity 'blocks' named entity 'disruption' named entity 'CNS' named entity 'α4β1' named entity 'virus' named entity 'meningoencephalitis' named entity 'DIFFERENTIAL' named entity 'MODULATION' named entity 'DISRUPTION' named entity 'T HELPER CELL' named entity 'NATALIZUMAB' named entity 'VACCINIA VIRUS' named entity 'PERFORIN-1' named entity 'CELLULAR' named entity 'IMMUNE CELLS' named entity 'SERIES' named entity 'CONTRAST' named entity 'ASSOCIATED WITH' named entity 'VIRAL INFECTIONS' named entity 'IMMUNE SURVEILLANCE' named entity 'RESULTS' named entity 'T CELL' named entity 'B14' named entity 'INTEGRINS' named entity 'VIRAL MENINGOENCEPHALITIS' named entity 'ANTI-INFLAMMATORY DRUGS' named entity 'SPECIFIC' named entity 'RECRUITMENT' named entity 'CONTROL' named entity 'VIRAL ENCEPHALITIS' named entity 'INTEGRIN' named entity 'IMMUNE RESPONSES' named entity 'NON-' named entity 'TH17 CELLS' named entity 'B14' named entity 'INTEGRINS' named entity 'GENERATE' named entity 'CYTOTOXIC' named entity 'TRAFFICKING' named entity 'PROPERTIES' named entity 'IMPAIRED' named entity 'POTENCY' named entity 'IMPAIR' named entity 'DEFICIENT' named entity 'B21' named entity 'CLEAR' named entity 'VLA-4' named entity 'EOMES' named entity 'INFECTION' named entity 'INFLAMMATORY' named entity 'BLOCKS' named entity 'CONDITIONAL' named entity 'THEIR' named entity 'VIRUS' named entity 'TH1 CELLS' named entity 'INTRATHECAL' named entity 'REDUNDANT' named entity 'EXPRESSION' named entity 'MICE' named entity 'HERE' named entity 'FAIL' named entity 'CNS' named entity 'DUE TO' named entity 'ADOPT' named entity 'IS A' named entity 'DIRECT' named entity 'INTRODUCTION' named entity 'INDUCED' named entity 'ACCESS' named entity 'ENTER' named entity 'AGENT'

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