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Infection and Immunity, January 2001, p. 245-251, Vol. 69, No. 1
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.1.245-251.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Vervet Monkeys Vaccinated with Killed Leishmania major Parasites and Interleukin-12 Develop a Type 1 Immune Response but Are Not Protected against Challenge Infection

Michael M. Gicheru,1 Joseph O. Olobo,1,dagger Christopher O. Anjili,2 Alloys S. Orago,3 Farrokh Modabber,4 and Phillip Scott5,*

Institute of Primate Research,1 Kenya Medical Research Institute,2 and Kenyatta University,3 Nairobi, Kenya; World Health Organization/TDR, Geneva, Switzerland4; and Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 191045

Received 30 May 2000/Returned for modification 21 July 2000/Accepted 29 September 2000

Leishmania major is a protozoan parasite that causes chronic cutaneous lesions that often leave disfiguring scars. Infections in mice have demonstrated that leishmanial vaccines that include interleukin-12 (IL-12) as an adjuvant are able to induce protective immunity. In this study, we assessed the safety, immunopotency, and adjuvant potential of two doses of IL-12 when used with a killed L. major vaccine in vervet monkeys. The induction of cell-mediated immunity following vaccination was determined by measuring delayed-type hypersensitivity, in vitro lymphocyte proliferation, and gamma interferon (IFN-gamma ) production. Protection was assessed by challenging the animals with L. major parasites and monitoring the course of infection. At low doses of IL-12 (10 µg), a small increase in the parameters of cell-mediated immunity was observed, relative to those in animals that received antigen without IL-12. However, none of these animals were protected against a challenge infection. At higher doses of IL-12 (30 µg), a substantial increase in Leishmania-specific immune responses was observed, and monkeys immunized with antigen and IL-12 exhibited an IFN-gamma response that was as great as that in animals that had resolved a primary infection and were immune. Nevertheless, despite the presence of correlates of protection, the disease course was only slightly altered, and protection was low compared to that in self-cured monkeys. These data suggest that protection against leishmaniasis may require more than the activation of Leishmania-specific IFN-gamma -producing T cells, which has important implications for designing a vaccine against leishmaniasis.

* Corresponding author. Mailing address: Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, 3800 Spruce St., Philadelphia, PA 19104. Phone: (215) 898-1602. Fax: (215) 573-7023. E-mail: pscott{at}vet.upenn.edu.

dagger Present address: Armauer Hansen Research Institute, Addis Ababa, Ethiopia.

Infection and Immunity, January 2001, p. 245-251, Vol. 69, No. 1
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.1.245-251.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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