Different genetic control of cutaneous and visceral disease after Leishmania major infection in mice
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
12654824
PubMed Central
PMC152088
DOI
10.1128/iai.71.4.2041-2046.2003
Knihovny.cz E-zdroje
- MeSH
- genetická predispozice k nemoci * MeSH
- genetická vazba MeSH
- genotyp MeSH
- hepatomegalie MeSH
- inbrední kmeny myší genetika MeSH
- křížení genetické MeSH
- Leishmania major patogenita MeSH
- leishmanióza kožní genetika imunologie patofyziologie MeSH
- leishmanióza viscerální genetika imunologie patofyziologie MeSH
- mapování chromozomů MeSH
- myši inbrední BALB C genetika MeSH
- myši MeSH
- splenomegalie MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
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)F(2) 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.
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