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Infection and Immunity, September 2002, p. 5075-5080, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.5075-5080.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Endogenous Interleukin-12 Is Critical for Controlling the Late but Not the Early Stage of Leishmania mexicana Infection in C57BL/6 Mice

Fabiola Aguilar Torrentera,1,2,{dagger} Jon D. Laman,3 Marjan Van Meurs,3 Luciano Adorini,4 Eric Muraille,1 and Y. Carlier1*

Laboratory of Parasitology, Free University of Brussels (ULB), Brussels, Belgium,1 Department of Immunology, Escuela Nacional de Ciencias Biologicas, Instituto Politecnico Nacional, Mexico DF, Mexico,2 Department of Immunology, Erasmus MC Rotterdam (EUR), Rotterdam, The Netherlands,3 Bioxell, Milano, Italy4

Received 29 April 2002/ Returned for modification 25 May 2002/ Accepted 11 June 2002

The role of interleukin-12 (IL-12) has been clearly established in the resistance of C57BL/6 (B6) mice to Leishmania major infection, but its involvement in the control of Leishmania mexicana infection remains to be determined. Here, we show the following. (i) L. mexicana, in contrast to L. major, induces the development of nonhealing lesions in B6 mice. (ii) Cells expressing IL-12p40, gamma interferon (IFN-{gamma}), NOS2, and CD40L are numerous in the footpad lesion and/or the draining popliteal lymph node of animals infected for up to 14 weeks with L. mexicana. (iii) B6 mice, either IL-12p40 deficient or treated with IL-12p40-neutralizing antibodies, display a dramatic enhancement of primary and secondary lesions leading to death 10 weeks after inoculation with L. mexicana. (iv) Splenocytes harvested 4 and 8 weeks after infection of IL-12p40-/- B6 mice with L. mexicana are unable to produce IFN-{gamma}, but secrete IL-4, IL-10, and IL-18. Thus, the early control of L. mexicana infection by B6 mice is independent of IL-12, whereas IL-12 and Th1 responses play a key role in controlling the late stages of L. mexicana infection. However, they fail to resolve lesions, in contrast to L. major infection, emphasizing the different outcomes induced by these two Leishmania species in B6 mice.

* Corresponding author. Mailing address: Laboratory of Parasitology, Faculty of Medicine, ULB, CP 616, Route de Lennik 808, B-1070 Brussels, Belgium. Phone: 32 2 555 62 55. Fax: 32 2 555 61 28. E-mail: ycarlier{at}ulb.ac.be.

Editor: W. A. Petri, Jr.

{dagger} Present address: Escuela Nacional de Ciencias Biologicas, Instituto Politecnico Nacional, Mexico DF, Mexico.

Infection and Immunity, September 2002, p. 5075-5080, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.5075-5080.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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