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

Author:

Chakkalath Hrishekesh R.1,Siddiqui Afzal A.1,Shankar Anuraj H.1,Dobson Deborah E.2,Beverley Stephen M.32,Titus Richard G.4

Affiliation:

1. Department of Tropical Public Health, Harvard School of Public Health,1 and

2. Department of Molecular Microbiology, Washington University Medical School, St. Louis, Missouri 631102; and

3. Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School,3 Boston, Massachusetts 02115;

4. Department of Pathology, School of Veterinary Medicine and Biological Sciences, Colorado State University, Fort Collins, Colorado 805234

Abstract

ABSTRACT 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 β-galactosidase (β-GAL); this parasite was designated L. major-βGAL . BALB/c and C3H mice responded to infection with L. major-βGAL by mounting a CD4 T-cell response to both parasite antigens and to the reporter antigen, β-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-βGAL by producing interleukin 4 in response to the parasite and C3H mice produced gamma interferon (IFN-γ) in response to the parasite and β-GAL. Interestingly, however, BALB/c mice produced IFN-γ in response to β-GAL. Taken together, these results demonstrate that priming of IFN-γ-producing cells can occur in BALB/c mice despite the fact the animals are simultaneously mounting a potent Th2 response to L. major .

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

Reference35 articles.

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