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The Journal of Immunology, 2003, 170: 5349-5353.
Copyright © 2003 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: Bradykinin Induces IL-12 Production by Dendritic Cells: A Danger Signal That Drives Th1 Polarization1

Julio Aliberti2,*, João P. B. Viola{dagger}, Adriana Vieira-de-Abreu{ddagger}, Patricia T. Bozza{ddagger}, Alan Sher* and Julio Scharfstein2,§

* Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892; and {dagger} Divisão de Medicina Experimental, Instituto Nacional de Câncer, {ddagger} Departamento de Fisiologia e Farmacodinâmica, Instituto Oswaldo Cruz, Fundaçao Oswaldo Cruz, and § Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil

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 B2 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 B2 bradykinin receptors.




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