The Journal of Experimental Medicine
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Published online 20 March 2000.
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© The Rockefeller University Press, 0022-1007/2000/3/1063/ $5.00
The Journal of Experimental Medicine, Volume 191, Number 6, March 20, 2000 1063-1068

Brief Definitive Report

Internalization of Leishmania mexicana Complex Amastigotes via the Fc Receptor Is Required to Sustain Infection in Murine Cutaneous Leishmaniasis

Peter E. Kimaa,d, Stephanie L. Constantb, Lynn Hannumb, Maria Colmenaresd, Karen S. Leeb, Ann M. Habermanc, Mark J. Shlomchikb,c, and Diane McMahon-Prattd

a Division of Microbial Pathogenesis, Yale University School of Medicine, New Haven, Connecticut 06520-8034
b Division of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8034
c Department of Laboratory Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8034
d Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut 06520-8034
Department of Epidemiology and Public Health, Yale University School of Medicine, 60 College St., LEPH 715, P.O. Box 208034, New Haven, CT 06520-8034.203-737-2921203-785-4481

diane.mcmahon-pratt{at}yale.edu

We show here that maintenance of Leishmania infections with Leishmania mexicana complex parasites (Leishmania amazonensis and Leishmania pifanoi) is impaired in the absence of circulating antibody. In these studies, we used mice genetically altered to contain no circulating antibody, with and without functional B cells. This experimental design allowed us to rule out a critical role for B cell antigen presentation in Leishmania pathogenesis. In addition, we show that mice lacking the common {gamma} chain of Fc receptors (Fc{gamma}RI, Fc{varepsilon}RI, and Fc{gamma}RIII) are similarly refractory to infection with these parasites. These observations establish a critical role for antibody in the pathogenesis associated with infection by members of the L. mexicana complex.

Key Words: Leishmania • Fc receptor • pathogenesis • antigen presentation • infection

P.E. Kima and S.L. Constant contributed equally to this work.

© 2000 The Rockefeller University Press


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