Refine
Has Fulltext
- yes (32)
Is part of the Bibliography
- yes (32)
Year of publication
Document Type
- Journal article (31)
- Doctoral Thesis (1)
Language
- English (32) (remove)
Keywords
- brain (32) (remove)
Institute
- Theodor-Boveri-Institut für Biowissenschaften (7)
- Klinik und Poliklinik für Psychiatrie, Psychosomatik und Psychotherapie (5)
- Neurochirurgische Klinik und Poliklinik (4)
- Pathologisches Institut (4)
- Institut für Psychologie (3)
- Klinik und Poliklinik für Kinder- und Jugendpsychiatrie, Psychosomatik und Psychotherapie (3)
- Neurologische Klinik und Poliklinik (3)
- Graduate School of Life Sciences (2)
- Institut für Anatomie und Zellbiologie (2)
- Klinik und Poliklinik für Anästhesiologie (ab 2004) (2)
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.