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Murine cerebral malaria development is independent of toll-like receptor signaling

Academic Article
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Overview

authors

  • Togbe, D.
  • Schofield, L.
  • Grau, G. E.
  • Schnyder, B.
  • Boissay, V.
  • Charron, S.
  • Rose, S.
  • Beutler, Bruce
  • Quesniaux, V. F. J.
  • Ryffel, B.

publication date

  • May 2007

journal

  • American Journal of Pathology  Journal

abstract

  • Malaria pigment hemozoin was reported to activate the innate immunity by Toll-like receptor (TLR)-9 engagement. However, the role of TLR activation for the development of cerebral malaria (CM), a lethal complication of malaria infection in humans, is unknown. Using Plasmodium berghei ANKA (PbA) infection in mice as a model of CM, we report here that TLR9-deficient mice are not protected from CM. To exclude the role of other members of the TLR family in PbA recognition, we infected mice deficient for single TLR1, -2, -3, -4, -6, -7, or -9 and their adapter proteins MyD88, TIRAP, and TRIF. In contrast to lymphotoxin alpha-deficient mice, which are resistant to CM, all TLR-deficient mice were as sensitive to fatal CM development as wild-type control mice and developed typical microvascular damage with vascular leak and hemorrhage in the brain and lung, together with comparable parasitemia, thrombocytopenia, neutrophilia, and lymphopenia. In conclusion, the present data do not exclude the possibility that malarial molecular motifs may activate the innate immune system. However, TLR-dependent activation of innate immunity is unlikely to contribute significantly to the proinflammatory response to PbA infection and the development of fatal CM.

subject areas

  • Animals
  • Brain
  • Capillaries
  • Enzyme-Linked Immunosorbent Assay
  • Flow Cytometry
  • Humans
  • Immunohistochemistry
  • Liver
  • Lung
  • Malaria, Cerebral
  • Mice
  • Plasmodium berghei
  • Signal Transduction
  • Toll-Like Receptors
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Identity

PubMed Central ID

  • PMC1854958

International Standard Serial Number (ISSN)

  • 0002-9440

Digital Object Identifier (DOI)

  • 10.2353/ajpath.2007.060889

PubMed ID

  • 17456769
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Additional Document Info

start page

  • 1640

end page

  • 1648

volume

  • 170

issue

  • 5

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