Geisy Monteiro | Universidade Federal do Rio de Janeiro (UFRJ) (original) (raw)

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Papers by Geisy Monteiro

Research paper thumbnail of Glucuronoxylomannan of Cryptococcus neoformans exacerbates in vitro yeast cell growth by interleukin 10-dependent inhibition of CD4 + T lymphocyte responses

Cellular Immunology, 2003

Glucuronoxylomannan (GXM), the major capsular polysaccharide of Cryptococcus neoformans, is the m... more Glucuronoxylomannan (GXM), the major capsular polysaccharide of Cryptococcus neoformans, is the most important virulence factor of this fungus. We analyzed the molecular events related to protective immune responses against a non-encapsulated strain of C. neoformans, mediated by murine splenic CD4 þ T lymphocytes in vitro, and the impact of GXM addition upon these events. Both the lymphoproliferation of CD4 þ T cells and the control of fungus growth were dependent on B7 co-stimulation. Addition of GXM did not modify CD4 þ T cell proliferation, but exacerbated infection in cultures obtained from normal and infected hosts. GXM enhanced the secretion of IL-10 and IL-4, while it reduced the production of pro-inflammatory cytokines TNF-a and IFN-c. The blockade of IL-10 activity with neutralizing antibodies increased TNF-a production and reduced yeast cell growth. The findings suggest that GXM exacerbates infection by down-regulating cell-mediated protective immune response and that IL-10 is implicated in yeast evasion.

Research paper thumbnail of Apoptotic lymphocytes treated with IgG from Trypanosoma cruzi infection increase TNF-α secretion and reduce parasite replication in macrophages

European Journal of Immunology, 2010

Phagocytic removal of apoptotic lymphocytes exacerbates replication of Trypanosoma cruzi in macro... more Phagocytic removal of apoptotic lymphocytes exacerbates replication of Trypanosoma cruzi in macrophages. We investigated the presence of Ab against apoptotic lymphocytes in T. cruzi infection and the role of these Ab in parasite replication. Both control and chagasic serum contained IgG Ab that opsonized apoptotic lymphocytes. Treatment of apoptotic lymphocytes with purified IgG from chagasic, but not control serum, reduced T. cruzi replication in macrophages. The protective effect of chagasic IgG depended on Fcγ receptors, as demonstrated by the requirement for the intact Fc portion of IgG, and the effect could be abrogated by treating macrophages with an anti-CD16/CD32 Fab fragment. Chagasic IgG displayed increased reactivity against a subset of apoptotic cell Ag, as measured by flow cytometry and immunoblot analyses. Apoptotic lymphocytes treated with chagasic IgG, but not control IgG, increased production of TNF-α, while decreasing production of TGF-β1 by infected macrophages. Increased control of parasite replication required TNF-α production. Previous immunization with apoptotic cells or injection of apoptotic cells opsonized with chagasic IgG reduced parasitemia in infected mice. These results indicate that Ab raised against apoptotic cells could play a protective role in control of T. cruzi replication by macrophages.

Research paper thumbnail of Glucuronoxylomannan of Cryptococcus neoformans exacerbates in vitro yeast cell growth by interleukin 10-dependent inhibition of CD4 + T lymphocyte responses

Cellular Immunology, 2003

Glucuronoxylomannan (GXM), the major capsular polysaccharide of Cryptococcus neoformans, is the m... more Glucuronoxylomannan (GXM), the major capsular polysaccharide of Cryptococcus neoformans, is the most important virulence factor of this fungus. We analyzed the molecular events related to protective immune responses against a non-encapsulated strain of C. neoformans, mediated by murine splenic CD4 þ T lymphocytes in vitro, and the impact of GXM addition upon these events. Both the lymphoproliferation of CD4 þ T cells and the control of fungus growth were dependent on B7 co-stimulation. Addition of GXM did not modify CD4 þ T cell proliferation, but exacerbated infection in cultures obtained from normal and infected hosts. GXM enhanced the secretion of IL-10 and IL-4, while it reduced the production of pro-inflammatory cytokines TNF-a and IFN-c. The blockade of IL-10 activity with neutralizing antibodies increased TNF-a production and reduced yeast cell growth. The findings suggest that GXM exacerbates infection by down-regulating cell-mediated protective immune response and that IL-10 is implicated in yeast evasion.

Research paper thumbnail of Apoptotic lymphocytes treated with IgG from Trypanosoma cruzi infection increase TNF-α secretion and reduce parasite replication in macrophages

European Journal of Immunology, 2010

Phagocytic removal of apoptotic lymphocytes exacerbates replication of Trypanosoma cruzi in macro... more Phagocytic removal of apoptotic lymphocytes exacerbates replication of Trypanosoma cruzi in macrophages. We investigated the presence of Ab against apoptotic lymphocytes in T. cruzi infection and the role of these Ab in parasite replication. Both control and chagasic serum contained IgG Ab that opsonized apoptotic lymphocytes. Treatment of apoptotic lymphocytes with purified IgG from chagasic, but not control serum, reduced T. cruzi replication in macrophages. The protective effect of chagasic IgG depended on Fcγ receptors, as demonstrated by the requirement for the intact Fc portion of IgG, and the effect could be abrogated by treating macrophages with an anti-CD16/CD32 Fab fragment. Chagasic IgG displayed increased reactivity against a subset of apoptotic cell Ag, as measured by flow cytometry and immunoblot analyses. Apoptotic lymphocytes treated with chagasic IgG, but not control IgG, increased production of TNF-α, while decreasing production of TGF-β1 by infected macrophages. Increased control of parasite replication required TNF-α production. Previous immunization with apoptotic cells or injection of apoptotic cells opsonized with chagasic IgG reduced parasitemia in infected mice. These results indicate that Ab raised against apoptotic cells could play a protective role in control of T. cruzi replication by macrophages.

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