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Maffia, Paulo César; Zittermann, Sandra Elizabeth; Scimone, María Lucila; Tateosian, Nancy; Amiano, Nicolás; Guerrieri, Diego; Lutzky, Viviana; Rosso, Diego; Romeo, Horacio Eduardo; Garcia, Verónica E; Issekutz, Andrew C; Chuluyan, H. Eduardo
The American journal of pathology, 2007, Volume: 171, Issue: 3Journal Article
During microbial infection, neutrophils (polymorphonuclear leukocytes; PMNs) activate dendritic cells (DCs). However, early reports illustrated that neutrophil-derived mediators may suppress responses to mitogens. In the present study, we investigated the mechanism used by PMNs to modulate the immunostimulatory ability of DCs. Autologous syngeneic PMNs decreased T-cell proliferation induced by allogeneic DCs. Culture supernatant (CS) derived from PMNs also decreased allostimulation ability of immature DCs and increased the expression of transforming growth factor (TGF)-β1 on DCs. A TGF-β1 monoclonal antibody, a CD40 monoclonal antibody, or a serine protease inhibitor reversed the effect of PMN CS on DC allostimulatory ability. Furthermore, elastase reproduced the inhibitory effect of PMN CS on DC allostimulatory ability and the TGF-β1 production. The role of elastase was confirmed by examining PMN CS from two patients with cyclic neutropenia, a disease due to mutations in the neutrophil elastase gene. These PMN CS samples had reduced elastase activity and were unable to increase DC TGF-β1 production. Moreover, elastase and PMN CS induced IκBα degradation in DCs. We conclude that PMNs decrease DC allostimulatory ability via production of elastase leading to a switch of immature DCs into TGF-β1-secreting cells.
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