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Infection and Immunity, February 2000, p. 809-814, Vol. 68, No. 2
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Priming of a beta -Galactosidase (beta -GAL)-Specific Type 1 Response in BALB/c Mice Infected with beta -GAL-Transfected Leishmania major

Hrishekesh R. Chakkalath,1 Afzal A. Siddiqui,1,dagger Anuraj H. Shankar,1,Dagger Deborah E. Dobson,2 Stephen M. Beverley,2,3 and Richard G. Titus4,*

Department of Tropical Public Health, Harvard School of Public Health,1 and Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School,3 Boston, Massachusetts 02115; Department of Molecular Microbiology, Washington University Medical School, St. Louis, Missouri 631102; and Department of Pathology, School of Veterinary Medicine and Biological Sciences, Colorado State University, Fort Collins, Colorado 805234

Received 20 September 1999/Returned for modification 22 October 1999/Accepted 10 November 1999

To determine whether an ongoing response to Leishmania major would affect the response to a non-cross-reacting, non-leishmanial antigen, susceptible BALB/c mice and resistant C3H mice were infected with L. major parasites expressing Escherichia coli beta -galactosidase (beta -GAL); this parasite was designated L. major-beta GAL. BALB/c and C3H mice responded to infection with L. major-beta GAL by mounting a CD4 T-cell response to both parasite antigens and to the reporter antigen, beta -GAL. The phenotypes of these T cells were characterized after generating T-cell lines from infected mice. As expected, BALB/c mice responded to infection with L. major-beta GAL by producing interleukin 4 in response to the parasite and C3H mice produced gamma interferon (IFN-gamma ) in response to the parasite and beta -GAL. Interestingly, however, BALB/c mice produced IFN-gamma in response to beta -GAL. Taken together, these results demonstrate that priming of IFN-gamma -producing cells can occur in BALB/c mice despite the fact the animals are simultaneously mounting a potent Th2 response to L. major.

* Corresponding author. Mailing address: Department of Pathology, CVMBS, Colorado State University, Fort Collins, CO 80523. Phone: (970) 491-4964. Fax: (970) 491-0603. E-mail: rtitus{at}cvmbs.colostate.edu.

dagger Present address: Department of Internal Medicine, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614.

Dagger Present address: Department of International Health, Johns Hopkins University School of Public Health and Hygiene, Baltimore, MD 21205.

Infection and Immunity, February 2000, p. 809-814, Vol. 68, No. 2
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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