INVESTIGADORES
SOTOMAYOR Claudia Elena
artículos
Título:
Abrogation of spontaneous liver tolerance during immune response to Candida albicans:
Autor/es:
RENNA MS; FIGUEREDO CM; RODRIGUEZ- GALÁN MC; ICELY PA; PERALTA RAMOS JM; CORREA SG; SOTOMAYOR CE
Revista:
INTERNATIONAL IMMUNOLOGY
Editorial:
OXFORD UNIV PRESS
Referencias:
Año: 2012 vol. 24 p. 315 - 325
ISSN:
0953-8178
Resumen:
Abstract
Hepatic mononuclear cells (HMC) are a heterogeneous population with innate immune properties
involved in the response to several pathogens. Herein, during the primary infection with Candida
albicans, we observed dynamic changes in CD31, NK1 and NKT1 intrahepatic lymphoid subsets and
albicans, we observed dynamic changes in CD31, NK1 and NKT1 intrahepatic lymphoid subsets and
Candida
albicans, we observed dynamic changes in CD31, NK1 and NKT1 intrahepatic lymphoid subsets and, we observed dynamic changes in CD31, NK1 and NKT1 intrahepatic lymphoid subsets and
15 a significant increase in the absolute number of antigen-presenting cells (APC). The liver tolerogenic
microenvironment sustained by higher levels of IL-10, transforming growth factor-b and IL-4 was
severely modified upon the robust IFN-g production after the fungal colonization. NKT cells purified
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
severely modified upon the robust IFN-g production after the fungal colonization. NKT cells purified
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
microenvironment sustained by higher levels of IL-10, transforming growth factor-b and IL-4 was
severely modified upon the robust IFN-g production after the fungal colonization. NKT cells purified
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
severely modified upon the robust IFN-g production after the fungal colonization. NKT cells purified
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
a significant increase in the absolute number of antigen-presenting cells (APC). The liver tolerogenic
microenvironment sustained by higher levels of IL-10, transforming growth factor-b and IL-4 was
severely modified upon the robust IFN-g production after the fungal colonization. NKT cells purified
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
severely modified upon the robust IFN-g production after the fungal colonization. NKT cells purified
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
b and IL-4 was
severely modified upon the robust IFN-g production after the fungal colonization. NKT cells purified
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unable
g production after the fungal colonization. NKT cells purified
from infected animals released significant amounts of IFN-gamma and the production of this cytokine
was exacerbated after a second contact with the fungus. Interestingly, C. albicans per se was unableC. albicans per se was unable
20 to activate tolerogenic NKT cells from naive animals. In vitro experiments performed with HMC cells
depleted of the CD11b/c1 population revealed that in the absence of APC, NKT cells are unable to
produce IFN-g in response to C. albicans. Our findings constitute the first evidence that this innate
lymphocyte population is involved in the pathogenesis of C. albicans infection.
lymphocyte population is involved in the pathogenesis of C. albicans infection.
produce IFN-g in response to C. albicans. Our findings constitute the first evidence that this innate
lymphocyte population is involved in the pathogenesis of C. albicans infection.
lymphocyte population is involved in the pathogenesis of C. albicans infection.
depleted of the CD11b/c1 population revealed that in the absence of APC, NKT cells are unable to
produce IFN-g in response to C. albicans. Our findings constitute the first evidence that this innate
lymphocyte population is involved in the pathogenesis of C. albicans infection.
lymphocyte population is involved in the pathogenesis of C. albicans infection.
produce IFN-g in response to C. albicans. Our findings constitute the first evidence that this innate
lymphocyte population is involved in the pathogenesis of C. albicans infection.
lymphocyte population is involved in the pathogenesis of C. albicans infection.
to activate tolerogenic NKT cells from naive animals. In vitro experiments performed with HMC cells
depleted of the CD11b/c1 population revealed that in the absence of APC, NKT cells are unable to
produce IFN-g in response to C. albicans. Our findings constitute the first evidence that this innate
lymphocyte population is involved in the pathogenesis of C. albicans infection.
lymphocyte population is involved in the pathogenesis of C. albicans infection.
produce IFN-g in response to C. albicans. Our findings constitute the first evidence that this innate
lymphocyte population is involved in the pathogenesis of C. albicans infection.
lymphocyte population is involved in the pathogenesis of C. albicans infection.
1 population revealed that in the absence of APC, NKT cells are unable to
produce IFN-g in response to C. albicans. Our findings constitute the first evidence that this innate
lymphocyte population is involved in the pathogenesis of C. albicans infection.
lymphocyte population is involved in the pathogenesis of C. albicans infection.
g in response to C. albicans. Our findings constitute the first evidence that this innate
lymphocyte population is involved in the pathogenesis of C. albicans infection.C. albicans infection.