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Infection and Immunity, April 2003, p. 2041-2046, Vol. 71, No. 4
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.4.2041-2046.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Different Genetic Control of Cutaneous and Visceral Disease after Leishmania major Infection in Mice

Vladimir Vladimirov,1,{dagger} Jana Badalová,1,2 Milena Svobodová,3 Helena Havelková,1 Augustinus A. M. Hart,4 Hana Blazková,1 Peter Demant,5,{ddagger} and Marie Lipoldová1,2*

Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, 166 37 Prague 6,1 3rd Faculty of Medicine, Charles University, 100 00 Prague 10,2 Department of Parasitology, Faculty of Science, Charles University, 128 44 Prague 2, Czech Republic,3 Division of Radiotherapy,4 Division of Molecular Genetics, The Netherlands Cancer Institute, 1066 CX Amsterdam, The Netherlands5

Received 21 October 2002/ Returned for modification 9 December 2002/ Accepted 9 January 2003

The mouse strains BALB/cHeA (BALB/c) and STS/A (STS) are susceptible and resistant to Leishmania major-induced disease, respectively. We analyzed this difference using recombinant congenic (RC) BALB/c-c-STS/Dem (CcS/Dem) strains that carry different random subsets of 12.5% genes of the strain STS in a BALB/c background. Previously, testing the resistant strain CcS-5, we found five novel Lmr (Leishmania major response) loci, each associated with a different combination of pathological and immunological reactions. Here we analyze the response of RC strain CcS-16, which is even more susceptible to L. major than BALB/c. In the (CcS-16 x BALB/c)F2 hybrids we mapped three novel loci that influence cutaneous or visceral pathology. Lmr14 (chromosome 2) controls splenomegaly and hepatomegaly. On the other hand Lmr15 (chromosome 11) determines hepatomegaly only, and Lmr13 (chromosome 18) determines skin lesions only. These data confirm the complex control of L. major-induced pathology, where cutaneous and visceral pathology are controlled by different combinations of genes. It indicates organ-specific control of antiparasite responses. The definition of genes controlling these responses will permit a better understanding of pathways and genetic diversity underlying the different disease phenotypes.

* Corresponding author. Mailing address: Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Fleming. nám. 2, 166 37 Prague 6, Czech Republic. Phone: (420) 224 310 195. Fax: (420) 224 310 955. E-mail: lipoldova{at}img.cas.cz.

Editor: S. H. E. Kaufmann

{dagger} Present address: Massey Cancer Center, Virginia Commonwealth University, Richmond, VA 23298.

{ddagger} Present address: Roswell Park Cancer Institute, Buffalo, NY 14263.

Infection and Immunity, April 2003, p. 2041-2046, Vol. 71, No. 4
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.4.2041-2046.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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