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

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

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We earlier established a model of a MADURA DEVELOPMENT PLAN AS A DESTINATION SYARIAH INDONESIA TOURISM 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 Publication Metrics and Subject Categories of Biomechanics Journals 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.