Foxp3+ regulatory T cells control persistence of viral CNS infection.
dc.contributor.author | Reuter, Dajana | |
dc.contributor.author | Sparwasser, Tim | |
dc.contributor.author | Hünig, Thomas | |
dc.contributor.author | Schneider-Schaulies, Jürgen | |
dc.date.accessioned | 2016-02-03T14:47:42Z | en |
dc.date.available | 2016-02-03T14:47:42Z | en |
dc.date.issued | 2012 | en |
dc.identifier.citation | Foxp3+ regulatory T cells control persistence of viral CNS infection. 2012, 7 (3):e33989 PLoS ONE | en |
dc.identifier.issn | 1932-6203 | en |
dc.identifier.pmid | 22448284 | en |
dc.identifier.doi | 10.1371/journal.pone.0033989 | en |
dc.identifier.uri | http://hdl.handle.net/10033/595526 | en |
dc.description.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. | |
dc.language.iso | en | en |
dc.subject.mesh | Animals | en |
dc.subject.mesh | Brain | en |
dc.subject.mesh | Central Nervous System Viral Diseases | en |
dc.subject.mesh | Cercopithecus aethiops | en |
dc.subject.mesh | Flow Cytometry | en |
dc.subject.mesh | Forkhead Transcription Factors | en |
dc.subject.mesh | Immunosuppression | en |
dc.subject.mesh | Measles | en |
dc.subject.mesh | Measles virus | en |
dc.subject.mesh | Mice | en |
dc.subject.mesh | Mice, Inbred C57BL | en |
dc.subject.mesh | T-Lymphocytes, Regulatory | en |
dc.subject.mesh | Vero Cells | en |
dc.title | Foxp3+ regulatory T cells control persistence of viral CNS infection. | en |
dc.type | Article | en |
dc.contributor.department | TWINCORE, Centre for Experimental and Clinical Infection Research GmbH, Feodor-Lynen-Str. 3-7, 30625 Hannover, Germany. | en |
dc.identifier.journal | PloS one | en |
refterms.dateFOA | 2018-06-13T04:11:02Z | |
html.description.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. |
Files in this item
This item appears in the following Collection(s)
-
publications of the TwinCore unit Infection immunology [80]
Publications of the Twincore Experimentelle Infektionsforschung