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CUTTING EDGE: BRADYKININ INDUCES IL-12 PRODUCTION BY DENDRITIC CELLS: A DANGER SIGNAL THAT DRIVES TH1 POLARIZATION
Autor
Afiliación
National Institutes of Health. National Institute of Allergy and Infectious Disease. Immunobiology Section. Bethesda, MD, USA.
Instituto Nacional de Câncer. Divisâo de Medicina Experimental. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Rio de Janeiro, RJ, Brasil.
National Institutes of Health. National Institute of Allergy and Infectious Disease. Immunobiology Section. Bethesda, MD, USA.
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.
Instituto Nacional de Câncer. Divisâo de Medicina Experimental. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Rio de Janeiro, RJ, Brasil.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Departamento de Fisiologia e Farmacodinâmica. Rio de Janeiro, RJ, Brasil.
National Institutes of Health. National Institute of Allergy and Infectious Disease. Immunobiology Section. Bethesda, MD, USA.
Universidade Federal do Rio de Janeiro. Instituto de Biofísica Carlos Chagas Filho. Rio de Janeiro, RJ, Brasil.
Resumen en ingles
Dendritic cells play a major role in the induction of both innate and acquired immune responses against pathogenic invaders. These cells are also able to sense endogenous activation signals liberated by injured tissues even in the absence of infection. In the present work, we demonstrate that kinins mobilize dendritic cells to produce IL-12 through activation of the B(2) bradykinin receptor subtype and that bradykinin-induced IL-12 responses are tightly regulated both by angiotensin-converting enzyme, a kinin-degrading peptidase, and by endogenous IL-10. Using a mouse model of allergic inflammation, we further show that addition of bradykinin to OVA during immunization results in decreased eosinophil infiltration on Ag challenge. The latter effect was demonstrated to be due to IL-12-driven skewing of Ag-specific T cell responses to a type 1 cytokine profile. Our data thus indicate that kinin peptides can serve as danger signals that trigger dendritic cells to produce IL-12 through activation of B(2) bradykinin receptors.
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