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Il-10 blockade facilitates DNA vaccine-induced t cell responses and enhances clearance of persistent virus infection

Academic Article
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Overview

authors

  • Brooks, D. G.
  • Lee, A. M.
  • Elsaesser, H.
  • McGavern, Dorian
  • Oldstone, Michael

publication date

  • March 2008

journal

  • Journal of Experimental Medicine  Journal

abstract

  • Therapeutic vaccination is a potentially powerful strategy to establish immune control and eradicate persistent viral infections. Large and multifunctional antiviral T cell responses are associated with control of viral persistence; however, for reasons that were mostly unclear, current therapeutic vaccination approaches to restore T cell immunity and control viral infection have been ineffective. Herein, we confirmed that neutralization of the immunosuppressive factor interleukin (IL)-10 stimulated T cell responses and improved control of established persistent lymphocytic choriomeningitis virus (LCMV) infection. Importantly, blockade of IL-10 also allowed an otherwise ineffective therapeutic DNA vaccine to further stimulate antiviral immunity, thereby increasing T cell responses and enhancing clearance of persistent LCMV replication. We therefore propose that a reason that current therapeutic vaccination strategies fail to resurrect/sustain T cell responses is because they do not alleviate the immunosuppressive environment. Consequently, blocking key suppressive factors could render ineffective vaccines more efficient at improving T cell immunity, and thereby allow immune-mediated control of persistent viral infection.

subject areas

  • Animals
  • Arenaviridae Infections
  • Immunosuppression
  • Interleukin-10
  • Lymphocytic choriomeningitis virus
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Receptors, Interleukin-10
  • T-Lymphocytes
  • Vaccination
  • Vaccines, DNA
  • Viral Vaccines
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Identity

PubMed Central ID

  • PMC2275377

International Standard Serial Number (ISSN)

  • 0022-1007

Digital Object Identifier (DOI)

  • 10.1084/jem.20071948

PubMed ID

  • 18332180
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Additional Document Info

start page

  • 533

end page

  • 541

volume

  • 205

issue

  • 3

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