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Interleukin-10 determines viral clearance or persistence in vivo

Academic Article
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Overview

authors

  • Brooks, D. G.
  • Trifilo, M. J.
  • Edelmann, K. H.
  • Teyton, Luc
  • McGavern, Dorian
  • Oldstone, Michael

publication date

  • November 2006

journal

  • Nature Medicine  Journal

abstract

  • Persistent viral infections are a major health concern. One obstacle inhibiting the clearance of persistent infections is functional inactivation of antiviral T cells. Although such immunosuppression occurs rapidly after infection, the mechanisms that induce the loss of T-cell activity and promote viral persistence are unknown. Herein we document that persistent viral infection in mice results in a significant upregulation of interleukin (IL)-10 by antigen-presenting cells, leading to impaired T-cell responses. Genetic removal of Il10 resulted in the maintenance of robust effector T-cell responses, the rapid elimination of virus and the development of antiviral memory T-cell responses. Therapeutic administration of an antibody that blocks the IL-10 receptor restored T-cell function and eliminated viral infection. Thus, we identify a single molecule that directly induces immunosuppression leading to viral persistence and demonstrate that a therapy to neutralize IL-10 results in T-cell recovery and the prevention of viral persistence.

subject areas

  • Animals
  • CD4-Positive T-Lymphocytes
  • CD8-Positive T-Lymphocytes
  • Flow Cytometry
  • HIV
  • Hepacivirus
  • Immunologic Memory
  • Interleukin-10
  • Lymphocytic choriomeningitis virus
  • Mice
  • Receptors, Interleukin-10
  • Reverse Transcriptase Polymerase Chain Reaction
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Identity

PubMed Central ID

  • PMC2535582

International Standard Serial Number (ISSN)

  • 1078-8956

Digital Object Identifier (DOI)

  • 10.1038/nm1492

PubMed ID

  • 17041596
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Additional Document Info

start page

  • 1301

end page

  • 1309

volume

  • 12

issue

  • 11

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