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Infection and Immunity, February 2002, p. 498-503, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.2.498-503.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Influence of Parasite Load on the Ability of Type 1 T Cells To Control Leishmania major Infection

Brian Hondowicz and Phillip Scott*

Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Received 2 May 2001/ Returned for modification 20 June 2001/ Accepted 23 October 2001

BALB/c mice infected with Leishmania major developed a type 2 immune response which failed to control parasite replication. We found that scid mice that received splenocytes from BALB/c mice that had been infected for 3 weeks with L. major (a type 2 cell population) and that were subsequently infected with L. major were protected when they were treated with interleukin 12 (IL-12). In contrast, IL-12 was ineffective at protecting BALB/c mice infected for 3 weeks, suggesting that a high parasite load regulates the development of protective immunity. To determine how this regulation operates, we performed a series of adoptive transfers of naïve, type 1 or type 2 splenocytes into scid mice. The recipient scid mice were infected either for 5 weeks prior to cell transfer (and thus had a high parasite load) or at the time of cell transfer. scid mice that were infected for 5 weeks and received a type 1 cell population were able to cure their lesions. However, when 5-week-infected scid mice received both type 1 and 2 cell populations, they were unable to control their infections. In contrast, the same type 1 and 2 cells transferred to naïve scid mice, which were subsequently infected, provided protection. In addition, we found that naïve cells mediated protection in scid mice with established lesions. These results show that high parasite numbers do not block type 1 protective responses or the development of type 1 responses. Instead, the influence of a high parasite load is dependent on the presence of a type 2 cell population.

* 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.

Editor: J. M. Mansfield

Infection and Immunity, February 2002, p. 498-503, Vol. 70, No. 2
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.2.498-503.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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