Abstract
Susceptibility to infection with Leishmania amazonensis promastigotes was examined in six B10 congenic mouse strains, including C57BL/10J (H2b), B10.BR (H2k), B10.M (H2f), B10.S (H2s), B10.RIII (H2r), and B10.D2 (H2d). All strains of mice developed skin nodules with punch-out ulcers by 8 weeks post-infection, but B10.M and B10.S mice showed resolution of cutaneous leishmaniasis lesions by 16 weeks post-infection. In addition, the skin lesions were much larger in BALB congenic mice than in B10 and C3H mice, even though these mice share the same H2 haplotypes. These results suggest that H2 complex controls the growth of L. amazonensis in cutaneous lesions, and that non-H2 genes inherited by BALB congenic mice have a more potent role than the H2 complex in lesion progression.
Published Version
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