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Genes Immun ; 5(2): 93-100, 2004 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-14668789

RESUMO

The severity of disease caused by infection with Leishmania major depends critically on the genetics of the host. Early induction of T helper (Th)1-type immune responses in the resistant C57BL/6 mice and Th2-type responses in the susceptible BALB/c mice are thought to determine cure or disease, respectively. We have previously mapped three host response loci in a genetic cross between C57BL/6 and BALB/c mice, and here we show definitively the involvement of these loci in disease severity using animals congenic for each of the loci. Surprisingly, in the late stage of infection when the difference in disease severity between congenic and parental mice was most pronounced, their cytokine profile correlated with the genetic background of the mice and not with the severity of disease. This indicates that the loci that we have mapped are acting by a mechanism independent of Th phenotype.


Assuntos
Interferon gama/genética , Interleucina-4/genética , Leishmania major , Leishmaniose Cutânea/imunologia , Fenótipo , Animais , Animais Congênicos , Cruzamentos Genéticos , Primers do DNA , Modelos Animais de Doenças , Fluorescência , Ligação Genética/genética , Genótipo , Interferon gama/metabolismo , Interleucina-4/metabolismo , Leishmaniose Cutânea/genética , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Especificidade da Espécie , Células Th1/imunologia , Células Th2/imunologia
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