Leishmaniasis host response loci (lmr1-3) modify disease severity through a Th1/Th2-independent pathway.

Elso, C M; Roberts, L J; Smyth, G K; Thomson, R J; Baldwin, T M; Foote, S J; Handman, E

Elso, C M; Roberts, L J; Smyth, G K; Thomson, R J; Baldwin, T M; Foote, S J; Handman, E.

Affiliation

Elso CM; The Walter and Eliza Hall Institute of Medical Research, Victoria, Australia.

Genes Immun ; 5(2): 93-100, 2004 Mar.

Article in En | MEDLINE | ID: mdl-14668789

Subject(s)

Interferon-gamma/genetics; Interleukin-4/genetics; Leishmania major; Leishmaniasis, Cutaneous/immunology; Phenotype; Animals; Animals, Congenic; Crosses, Genetic; DNA Primers; Disease Models, Animal; Fluorescence; Genetic Linkage/genetics; Genotype; Interferon-gamma/metabolism; Interleukin-4/metabolism; Leishmaniasis, Cutaneous/genetics; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Species Specificity; Th1 Cells/immunology; Th2 Cells/immunology

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Collection: 01-internacional Database: MEDLINE Main subject: Phenotype / Interleukin-4 / Interferon-gamma / Leishmaniasis, Cutaneous / Leishmania major Type of study: Prognostic_studies Limits: Animals Language: En Journal: Genes Immun Journal subject: ALERGIA E IMUNOLOGIA / BIOLOGIA MOLECULAR Year: 2004 Document type: Article Affiliation country: Australia Country of publication: United kingdom

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