
pmid: 15094168
The objective of this study was to analyse hepatic cellular immune response of mice with "cure" and "non-cure" phenotypes to Leishmania infantum infection. During infection establishment, elevated TGF-beta levels and absence of a Th1 response may have contributed to parasite multiplication and to similar hepatic parasitic loads. Later in infection, an increase in the number and activation levels of CD8+ cells was observed simultaneously with parasite elimination, but only significant in "cure" strain. During this recovering phase, "non-cure" animals showed low Th2 cytokine levels, while TGF-beta production was higher than in "cure" mice. These results point out to a role for CD8+ T cells in liver acquired immune response and to TGF-beta regulation of "cure" and "non-cure" phenotype to L. infantum infection.
CD4-Positive T-Lymphocytes, Mesocricetus, CD4-CD8 Ratio, Antibodies, Protozoan, CD8-Positive T-Lymphocytes, Th1 Cells, Mice, Mice, Congenic, Th2 Cells, Liver, Transforming Growth Factor beta, Cricetinae, Animals, Cytokines, Leishmaniasis, Visceral, Leishmania infantum
CD4-Positive T-Lymphocytes, Mesocricetus, CD4-CD8 Ratio, Antibodies, Protozoan, CD8-Positive T-Lymphocytes, Th1 Cells, Mice, Mice, Congenic, Th2 Cells, Liver, Transforming Growth Factor beta, Cricetinae, Animals, Cytokines, Leishmaniasis, Visceral, Leishmania infantum
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