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2030-01-01
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- IOC - Artigos de Periódicos [12488]
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REGULATORY IGDHI B CELLS SUPPRESS T CELL FUNCTION VIA IL-10 AND PD-L1 DURING PROGRESSIVE VISCERAL LEISHMANIASIS
Autor
Afiliación
University of Iowa College of Public Health. Department of Epidemiology. Iowa City, Iowa, USA.
University of Iowa College of Public Health. Department of Epidemiology. Iowa City, Iowa, USA.
University of Iowa College of Public Health. Department of Epidemiology. Iowa City, Iowa, USA.
Universidade Federal do Rio Grande do Norte. Instituto de Medicina Tropical. Departamento de Bioquímica. Programa de Pós-Graduação em Saúde. Natal, RN, Brasil / Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório Interdisciplinar de Pesquisas Médicas. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Rio Grande do Norte. Instituto de Medicina Tropical. Departamento de Bioquímica. Programa de Pós-Graduação em Saúde. Natal, RN, Brasil / Secretaria de Estado de Saúde. Centro de Zoonoses. Natal, RN, Brasil.
Universidade Federal do Rio Grande do Norte. Instituto de Medicina Tropical. Departamento de Bioquímica. Programa de Pós-Graduação em Saúde. Natal, RN, Brasil.
University of Iowa Carver College of Medicine. Immunology Program. Iowa City, Iowa, USA.
University of Iowa Carver College of Medicine. Immunology Program. Iowa City, Iowa, USA.
University of Iowa Carver College of Medicine. Immunology Program. Iowa City, Iowa, USA.
University of Iowa College of Public Health. Department of Epidemiology. Iowa City, Iowa, USA.
University of Iowa College of Public Health. Department of Epidemiology. Iowa City, Iowa, USA.
University of Iowa College of Public Health. Department of Epidemiology. Iowa City, Iowa, USA.
Universidade Federal do Rio Grande do Norte. Instituto de Medicina Tropical. Departamento de Bioquímica. Programa de Pós-Graduação em Saúde. Natal, RN, Brasil / Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório Interdisciplinar de Pesquisas Médicas. Rio de Janeiro, RJ, Brasil.
Universidade Federal do Rio Grande do Norte. Instituto de Medicina Tropical. Departamento de Bioquímica. Programa de Pós-Graduação em Saúde. Natal, RN, Brasil / Secretaria de Estado de Saúde. Centro de Zoonoses. Natal, RN, Brasil.
Universidade Federal do Rio Grande do Norte. Instituto de Medicina Tropical. Departamento de Bioquímica. Programa de Pós-Graduação em Saúde. Natal, RN, Brasil.
University of Iowa Carver College of Medicine. Immunology Program. Iowa City, Iowa, USA.
University of Iowa Carver College of Medicine. Immunology Program. Iowa City, Iowa, USA.
University of Iowa Carver College of Medicine. Immunology Program. Iowa City, Iowa, USA.
University of Iowa College of Public Health. Department of Epidemiology. Iowa City, Iowa, USA.
Resumen en ingles
During visceral leishmaniasis (VL), Th1-based inflammation is induced to control intracellular parasites. Inflammation-based pathology was shown to be dampened by IL-10 and eventual programmed death 1-mediated T cell exhaustion. Cell type(s) responsible for the initiation of T cell-produced IL-10 during VL are unknown. CD19(+), CD5(-), CD1d(-), IgD(hi) regulatory B cells from healthy controls produced IL-10 in the absence of infection or stimulation, in contrast to IgD(lo/neg) B cells. IgD(hi) B cells may have a de novo versus induced regulatory program. The population of IgD(hi) B cells increased 3-fold as VL progressed. B cells from VL dogs were necessary and sufficient to suppress Th1 cell effector function. IgD(hi) B cells induced IL-10 production by T cells and IgD(lo) B cells. Blockage of B cell-specific PD-L1 restored Th1 responses. IgD(hi) regulatory B cells represent a novel regulatory B cell that may precipitate T cell exhaustion during VL.
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