Data/hora: 09/06/2024 06:14:59

Provedor de dados: 	42	
País: 	Brazil	
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	
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.	
Data: 	2008-03-01	
Ano: 	2008	
Palavras-chave: 	Toxoplasma gondii strains; Innate immunity; Acquired immunity; TLR and MHC.	
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.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652008000100005	
Editor: 	Academia Brasileira de Ciências	
Relação: 	10.1590/S0001-37652008000100005	
Formato: 	text/html	
Fonte: 	Anais da Academia Brasileira de Ciências  v.80 n.1 2008	
Fonte: 	info:eu-repo/semantics/openAccess