Myeloid differentiation factor 88 is required for resistance to Neospora caninum infection

Open Access Option

Free access article

Issue		Vet. Res. Volume 40, Number 4, July-August 2009


Number of page(s)		12
DOI		10.1051/vetres/2009015
Published online		03 April 2009
How to cite this article		Vet. Res. (2009) 40:32

How to cite this article: Vet. Res. (2009) 40:32
DOI: 10.1051/vetres/2009015

Myeloid differentiation factor 88 is required for resistance to Neospora caninum infection

Tiago W.P. Mineo^{1, 2}, Luciana Benevides¹, Neide M. Silva² and João S. Silva¹

¹ Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, Av. Bandeirantes, 3900 - Ribeirão Preto, SP, Brazil
² Institute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, MG, Brazil

Received 5 August 2008; accepted 27 March 2009; published online 03 April 2009

Abstract - Neospora caninum is an intracellular parasite that causes major economic impact on cattle raising farms, and infects a wide range of warm-blooded hosts worldwide. Innate immune mechanisms that lead to protection against this parasite are still unknown. In order to investigate whether myeloid differentiation factor 88 (MyD88) is required for resistance against N. caninum, genetically deficient mice (MyD88^-/-) and wild type littermates were infected with live tachyzoites and the resistance to infection was evaluated. We found that sub-lethal tachyzoite doses induced acute mortality of MyD88^-/- mice, which succumbed to infection due to uncontrolled parasite replication. Higher parasitism in MyD88^-/- mice was associated with the lack of IL-12 production by dendritic cells, delayed IFN- $\gamma$ responses by NKT, CD4⁺ and CD8⁺ T lymphocytes, and production of high levels of IL-10. MyD88^-/- mice replenished with IL-12 and IFN- $\gamma$ abolished susceptibility as the animals survived throughout the experimental period. We conclude that protective IFN- $\gamma$ -mediated immunity to N. caninum is dependent on initial MyD88 signaling, in a mechanism triggered by production of IL-12 by dendritic cells. Further knowledge on Toll-like receptor recognition of N. caninum antigens is encouraged, since it could generate new prophylactic and therapeutic tools to control parasite burden.

Key words: Neospora caninum / innate immunity / MyD88 / IL-12 / IFN- $\gamma$

Corresponding author: tiago.mineo@pq.cnpq.br jsdsilva@fmrp.usp.br

© INRA, EDP Sciences 2009

What is OpenURL?

The OpenURL standard is a protocol for transmission of metadata describing the resource that you wish to access. An OpenURL link contains article metadata and directs it to the OpenURL server of your choice. The OpenURL server can provide access to the resource and also offer complementary services (specific search engine, export of references...). The OpenURL link can be generated by different means.

If your librarian has set up your subscription with an OpenURL resolver, OpenURL links appear automatically on the abstract pages.
You can define your own OpenURL resolver with your EDPS Account. In this case your choice will be given priority over that of your library.
You can use an add-on for your browser (Firefox or I.E.) to display OpenURL links on a page (see http://www.openly.com/openurlref/). You should disable this module if you wish to use the OpenURL server that you or your library have defined.