Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/348929
Type: Artigo
Title: Hypoxia modulates phenotype, inflammatory response, and leishmanial infection of human dendritic cells
Author: Bosseto, Maira Cegatti
Bonini Palma, Patricia Vianna
Covas, Dimas Tadeu
Giorgio, Selma
Abstract: Development of hypoxic areas occurs during infectious and inflammatory processes and dendritic cells (DCs) are involved in both innate and adaptive immunity in diseased tissues. Our group previously reported that macrophages exposed to hypoxia were infected with the intracellular parasite Leishmania amazonensis, but showed reduced susceptibility to the parasite. This study shows that although hypoxia did not alter human DC viability, it significantly altered phenotypic and functional characteristics. The expression of CD1a, CD80, and CD86 was significantly reduced in DCs exposed to hypoxia, whereas CD11c, CD14, CD123, CD49 and HLA-DR expression remained unaltered in DCs cultured in hypoxia or normoxia. DC secretion of IL-12p70, the bioactive interleukin-12 (IL-12), a cytokine produced in response to inflammatory mediators, was enhanced under hypoxia. In addition, phagocytic activity (Leishmania uptake) was not impaired under hypoxia, although this microenviroment induced infected DCs to reduce parasite survival, consequently controlling the infection rate. All these data support the notion that a hypoxic microenvironment promotes selective pressure on DCs to assume a phenotype characterized by pro-inflammatory and microbial activities in injured or inflamed tissues and contribute to the innate immune response
Subject: Células dendríticas
Leishmaniose
Hipóxia
Country: Estados Unidos
Editor: John Wiley & Sons
Rights: Fechado
Identifier DOI: 10.1111/j.1600-0463.2009.02568.x
Address: https://onlinelibrary.wiley.com/doi/full/10.1111/j.1600-0463.2009.02568.x
Date Issue: 2010
Appears in Collections:IB - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
000273883500004.pdf222.46 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.