About: Extralymphatic virus sanctuaries as a consequence of potent T-cell activation

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About: Extralymphatic virus sanctuaries as a consequence of potent T-cell activation Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Extralymphatic virus sanctuaries as a consequence of potent T-cell activation
Creator	Hangartner, Lars Fink, Katja Eschli, Bruno Hengartner, Hans Zinkernagel, Rolf Bergthaler, Andreas Hunziker, Lukas Merkler, Doron Recher, Mike Hegazy, Ahmed Lang, Karl Lang, Philipp Freigang, Stefan Georgiev, Panco Hersberger, Martin Jeker, Lukas Navarini, Alexander Odermatt, Bernhard Theocharides, Alexandre Zellweger, Raphael
Source	PMC
abstract	T helper cells can support the functions of CD8(+) T cells against persistently infecting viruses such as murine lymphocytic choriomeningitis virus (LCMV), cytomegalovirus, hepatitis C virus and HIV. These viruses often resist complete elimination and remain detectable at sanctuary sites, such as the kidneys and other extralymphatic organs. The mechanisms underlying this persistence are not well understood. Here we show that mice with potent virus-specific T-cell responses have reduced levels and delayed formation of neutralizing antibodies, and these mice fail to clear LCMV from extralymphatic epithelia. Transfer of virus-specific B cells but not virus-specific T cells augmented virus clearance from persistent sites. Virus elimination from the kidneys was associated with the formation of IgG deposits in the interstitial space, presumably from kidney-infiltrating B cells. CD8(+) T cells in the kidneys of mice that did not clear virus from this site were activated but showed evidence of exhaustion. Thus, we conclude that in this model of infection, site-specific virus persistence develops as a consequence of potent immune activation coupled with reductions in virus-specific neutralizing antibodies. Our results suggest that sanctuary-site formation depends both on organ anatomy and on the induction of different adaptive immune effector mechanisms. Boosting T-cell responses alone may not reduce virus persistence. SUPPLEMENTARY INFORMATION: The online version of this article (doi:10.1038/nm1670) contains supplementary material, which is available to authorized users.
has issue date	2007-11-04(xsd:dateTime)
bibo:doi	10.1038/nm1670
bibo:pmid	17982463
has license	no-cc
sha1sum (hex)	02beed2dafa4fa3f5d0bb8f91c9ab8a1966e6ed6
schema:url	https://doi.org/10.1038/nm1670
resource representing a document's title	Extralymphatic virus sanctuaries as a consequence of potent T-cell activation
has PubMed Central identifier	PMC7096094
has PubMed identifier	17982463
schema:publication	Nat Med
resource representing a document's body	covid:02beed2dafa4fa3f5d0bb8f91c9ab8a1966e6ed6#body_text
is schema:about of	named entity 'remain' named entity 'complete' named entity 'infecting' named entity 'mechanisms' named entity 'CD8' named entity 'T HELPER CELLS' named entity 'UNDERSTOOD' named entity 'VIRUS' named entity 'COMPLETE' named entity 'T CELLS' named entity 'HERE' named entity 'SUGGEST' named entity 'ADAPTIVE' named entity 'B CELLS' named entity 'KIDNEYS' named entity 'IGG' named entity 'ELIMINATION' named entity 'VIRUSES' named entity 'REDUCE' named entity 'FUNCTIONS' named entity 'LCMV' named entity 'IMMUNE ACTIVATION' named entity 'DEVELOPS' named entity 'UNDERLYING' named entity 'ACTIVATED' named entity 'OUR' named entity 'FAIL' named entity 'CYTOMEGALOVIRUS' named entity 'SITE' named entity 'THESE' named entity 'HAVE' named entity 'CONCLUDE' named entity 'INTERSTITIAL SPACE' named entity 'SUPPORT' named entity 'SPECIFIC' named entity 'ASSOCIATED WITH' named entity 'INFECTION' named entity 'BOOSTING' named entity 'CONSEQUENCE OF' named entity 'VIRUS' named entity 'RESPONSES' named entity 'MECHANISMS' named entity 'KIDNEY' named entity 'FORMATION' named entity 'SITES' named entity 'PERSISTENT' named entity 'ANATOMY' named entity 'MICE' named entity 'RESULTS' named entity 'COUPLED' named entity 'HEPATITIS C VIRUS' named entity 'T-CELL ACTIVATION' named entity 'DID' named entity 'LEVELS' named entity 'LYMPHOCYTIC CHORIOMENINGITIS VIRUS' named entity 'MURINE' named entity 'VIRUS CLEARANCE' named entity 'EFFECTOR' named entity 'REDUCED' named entity 'INFECTING' named entity 'PERSISTENCE' named entity 'INDUCTION'

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