Foxp3+ regulatory T cells control persistence of viral CNS infection.

2.50
Hdl Handle:
http://hdl.handle.net/10033/595526
Title:
Foxp3+ regulatory T cells control persistence of viral CNS infection.
Authors:
Reuter, Dajana; Sparwasser, Tim; Hünig, Thomas; Schneider-Schaulies, Jürgen
Abstract:
We earlier established a model of a persistent viral CNS infection using two week old immunologically normal (genetically unmodified) mice and recombinant measles virus (MV). Using this model infection we investigated the role of regulatory T cells (Tregs) as regulators of the immune response in the brain, and assessed whether the persistent CNS infection can be modulated by manipulation of Tregs in the periphery. CD4(+) CD25(+) Foxp3(+) Tregs were expanded or depleted during the persistent phase of the CNS infection, and the consequences for the virus-specific immune response and the extent of persistent infection were analyzed. Virus-specific CD8(+) T cells predominantly recognising the H-2D(b)-presented viral hemagglutinin epitope MV-H(22-30) (RIVINREHL) were quantified in the brain by pentamer staining. Expansion of Tregs after intraperitoneal (i.p.) application of the superagonistic anti-CD28 antibody D665 inducing transient immunosuppression caused increased virus replication and spread in the CNS. In contrast, depletion of Tregs using diphtheria toxin (DT) in DEREG (depletion of regulatory T cells)-mice induced an increase of virus-specific CD8(+) effector T cells in the brain and caused a reduction of the persistent infection. These data indicate that manipulation of Tregs in the periphery can be utilized to regulate virus persistence in the CNS.
Affiliation:
TWINCORE, Centre for Experimental and Clinical Infection Research GmbH, Feodor-Lynen-Str. 3-7, 30625 Hannover, Germany.
Citation:
Foxp3+ regulatory T cells control persistence of viral CNS infection. 2012, 7 (3):e33989 PLoS ONE
Journal:
PloS one
Issue Date:
2012
URI:
http://hdl.handle.net/10033/595526
DOI:
10.1371/journal.pone.0033989
PubMed ID:
22448284
Type:
Article
Language:
en
ISSN:
1932-6203
Appears in Collections:
publications of the TwinCore unit Infection immunology

Full metadata record

DC FieldValue Language
dc.contributor.authorReuter, Dajanaen
dc.contributor.authorSparwasser, Timen
dc.contributor.authorHünig, Thomasen
dc.contributor.authorSchneider-Schaulies, Jürgenen
dc.date.accessioned2016-02-03T14:47:42Zen
dc.date.available2016-02-03T14:47:42Zen
dc.date.issued2012en
dc.identifier.citationFoxp3+ regulatory T cells control persistence of viral CNS infection. 2012, 7 (3):e33989 PLoS ONEen
dc.identifier.issn1932-6203en
dc.identifier.pmid22448284en
dc.identifier.doi10.1371/journal.pone.0033989en
dc.identifier.urihttp://hdl.handle.net/10033/595526en
dc.description.abstractWe earlier established a model of a persistent viral CNS infection using two week old immunologically normal (genetically unmodified) mice and recombinant measles virus (MV). Using this model infection we investigated the role of regulatory T cells (Tregs) as regulators of the immune response in the brain, and assessed whether the persistent CNS infection can be modulated by manipulation of Tregs in the periphery. CD4(+) CD25(+) Foxp3(+) Tregs were expanded or depleted during the persistent phase of the CNS infection, and the consequences for the virus-specific immune response and the extent of persistent infection were analyzed. Virus-specific CD8(+) T cells predominantly recognising the H-2D(b)-presented viral hemagglutinin epitope MV-H(22-30) (RIVINREHL) were quantified in the brain by pentamer staining. Expansion of Tregs after intraperitoneal (i.p.) application of the superagonistic anti-CD28 antibody D665 inducing transient immunosuppression caused increased virus replication and spread in the CNS. In contrast, depletion of Tregs using diphtheria toxin (DT) in DEREG (depletion of regulatory T cells)-mice induced an increase of virus-specific CD8(+) effector T cells in the brain and caused a reduction of the persistent infection. These data indicate that manipulation of Tregs in the periphery can be utilized to regulate virus persistence in the CNS.en
dc.language.isoenen
dc.subject.meshAnimalsen
dc.subject.meshBrainen
dc.subject.meshCentral Nervous System Viral Diseasesen
dc.subject.meshCercopithecus aethiopsen
dc.subject.meshFlow Cytometryen
dc.subject.meshForkhead Transcription Factorsen
dc.subject.meshImmunosuppressionen
dc.subject.meshMeaslesen
dc.subject.meshMeasles virusen
dc.subject.meshMiceen
dc.subject.meshMice, Inbred C57BLen
dc.subject.meshT-Lymphocytes, Regulatoryen
dc.subject.meshVero Cellsen
dc.titleFoxp3+ regulatory T cells control persistence of viral CNS infection.en
dc.typeArticleen
dc.contributor.departmentTWINCORE, Centre for Experimental and Clinical Infection Research GmbH, Feodor-Lynen-Str. 3-7, 30625 Hannover, Germany.en
dc.identifier.journalPloS oneen

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