science pharmaceutical expo biotech jobs
Originally published online as doi:10.1189/jlb.1003484 on March 23, 2004

Published online before print March 23, 2004
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jlb.1003484v1
76/1/48    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kropf, P.
Right arrow Articles by Müller, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kropf, P.
Right arrow Articles by Müller, I.
(Journal of Leukocyte Biology. 2004;76:48-57.)
© 2004 by Society for Leukocyte Biology

Infection of C57BL/10ScCr and C57BL/10ScNCr mice with Leishmania major reveals a role for Toll-like receptor 4 in the control of parasite replication

P. Kropf*, N. Freudenberg{dagger}, C. Kalis{ddagger}, M. Modolell{ddagger}, S. Herath*, C. Galanos{ddagger}, M. Freudenberg{ddagger} and I. Müller*,1

* Imperial College London, Faculty of Medicine, Department of Immunology, United Kingdom;
{dagger} Institute of Pathology, University Hospital Freiburg, Germany; and
{ddagger} Max-Planck-Institute for Immunbiology, Freiburg, Germany

1Correspondence: Imperial College London, Faculty of Medicine, Division of Investigative Science, Department of Immunology, Norfolk Place, London, W2 1PG, United Kingdom. E-mail: i.muller{at}imperial.ac.uk

The innate immune system is essential for host defense; it senses the presence of potentially pathogenic-invading microorganisms, and the contribution of Toll-like receptors (TLRs) to this response is increasingly recognized. In the present study, we investigated the contribution of TLR4 to the course of cutaneous leishmaniasis in vivo. We used C57BL/10ScNCr (TLR40/0) and C57BL/10ScCr [TLR4/interleukin-12 (IL-12)Rß20/0] mice and compared the course of Leishmania major infection, parasite load, cell recruitment, and cytokine profile with those of wild-type C57BL/10ScSn mice. Our results confirm the importance of IL-12 receptor-mediated signaling in resistance to L. major infections. Importantly, we show that the lack of TLR4 results in an increased permissiveness for parasite growth during the innate and adaptive phase of the immune response and in delayed healing of the cutaneous lesions. The use of the tlr4 transgenic mouse strain TCr5 demonstrated unequivocally that TLR4 contributes to the efficient control of Leishmania growth in vivo.

Key Words: TLR4 • IL-12Rß2 • Leishmania




This article has been cited by other articles:


Home page
 Infect. Immun.Home page
F. F. Tuon, V. S. Amato, H. A. Bacha, T. AlMusawi, M. I. Duarte, and V. Amato Neto
Toll-Like Receptors and Leishmaniasis
Infect. Immun., March 1, 2008; 76(3): 866 - 872.
[Full Text] [PDF]

Home page
 J. Immunol.Home page
F. L. Ribeiro-Gomes, M. C. A. Moniz-de-Souza, M. S. Alexandre-Moreira, W. B. Dias, M. F. Lopes, M. P. Nunes, G. Lungarella, and G. A. DosReis
Neutrophils Activate Macrophages for Intracellular Killing of Leishmania major through Recruitment of TLR4 by Neutrophil Elastase
J. Immunol., September 15, 2007; 179(6): 3988 - 3994.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
S. Divanovic, A. Trompette, L. K. Petiniot, J. L. Allen, L. M. Flick, Y. Belkaid, R. Madan, J. J. Haky, and C. L. Karp
Regulation of TLR4 signaling and the host interface with pathogens and danger: the role of RP105
J. Leukoc. Biol., August 1, 2007; 82(2): 265 - 271.
[Abstract] [Full Text] [PDF]