TY  - JOUR
A1  - Reuter, Dajana
A1  - Sparwasser, Tim
A1  - Hünig, Thomas
A1  - Schneider-Schaulies, Jürgen
T1  - Foxp3\(^+\) Regulatory T Cells Control Persistence of Viral CNS Infection
JF  - PLoS One
N2  - 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-H22-30 (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.
KW  - antigen presentation
KW  - brain
KW  - central-nervous-system
KW  - virus-induced encephalitis
KW  - retroviral infection
KW  - gamma-interferon
KW  - measles virus
KW  - subacute sclerosing-panencephalitis
KW  - mice
KW  - CD4(+)
Y1  - 2012
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-134248
VL  - 7
IS  - 3
ER  -