| Registro completo |
| Provedor de dados: |
Anais da ABC (AABC)
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| País: |
Brazil
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| Título: |
The role of MHC haplotypes H2d/H2b in mouse resistance/susceptibility to cyst formation is influenced by the lineage of infective Toxoplasma gondii strain
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| Autores: |
Resende,Marianne G.
Fux,Blima
Caetano,Brália C.
Mendes,Erica A.
Silva,Neide M.
Ferreira,Adriana M.
Melo,Maria Norma
Vitor,Ricardo W.A.
Gazzinelli,Ricardo T.
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| Data: |
2008-03-01
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| Ano: |
2008
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| Palavras-chave: |
Toxoplasma gondii strains
Innate immunity
Acquired immunity
TLR and MHC
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| Resumo: |
Toxoplasma gondii strains displaying the Type I/III genotype are associated with acquired ocular toxoplasmosis in humans. Here, we used a mice model to characterize some immunological mechanisms involved in host resistance to infection with such strains. We have chosen the Type I/III strains D8, G2 and P-Br, which cause a chronic infection in mice that resembles human toxoplamosis. Mice deficient of molecules MyD88, IFN-gamma, and IL-12 were susceptible to all three parasite strains. This finding indicates the importance of innate mechanisms in controlling infection. On the other hand, MHC haplotype did not influenced resistance/susceptibility; since mice lineages displaying a same genetic background but different MHC haplotypes (H2b or H2d) developed similar mortality and cyst numbers after infection with those strains. In contrast, the C57BL/6 genetic background, and not MHC haplotype, was critical for development of intestinal inflammation caused by any of the studied strains. Finally, regarding effector mechanisms, weobserved that B and CD8+ T lymphocytes controlled survival,whereas the inducible nitric oxide synthase influenced cyst numbers in brains of mice infected with Type I/III strains. These findings are relevant to further understanding of the immunologic mechanisms involved in host protection and pathogenesis during infection with T. gondii.
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| Tipo: |
Info:eu-repo/semantics/article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652008000100005
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| Editor: |
Academia Brasileira de Ciências
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| Relação: |
10.1590/S0001-37652008000100005
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| Formato: |
text/html
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| Fonte: |
Anais da Academia Brasileira de Ciências v.80 n.1 2008
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| Direitos: |
info:eu-repo/semantics/openAccess
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