Please use this identifier to cite or link to this item:
Type: Artigo de periódico
Title: Ifn-β, Ifn-γ, And Tnf-α Decrease Erythrophagocytosis By Human Monocytes Independent Of Sirp-α Or Shp-1 Expression.
Author: de Almeida, Ana Carolina
Barbosa, Soraya Massaro
de Lourdes Rios Barjas-Castro, Maria
Olalla-Saad, Sara Terezinha
Condino-Neto, Antonio
Abstract: Many cases of autoimmune hemolytic anemia have been reported after viral infection. Phagocyte activation and accompanying erythrophagocytosis are thought to result from proinflammatory cytokines released during viral infection. SIRP-α (signal regulatory protein-α), a receptor expressed on phagocytes, inhibits phagocytosis when bound to CD47 on the erythrocyte membrane. Ligation with CD47 results in SHP-1 recruitment to SIRP-α and dephosphorylation of specific downstream substrates involved in phagocytosis. SIRP-α ligation by CD47 may be inhibited by proinflammatory cytokines. The aim of this work was to evaluate the effect of IFN-β, IFN-γ, and TNF-α on erythrophagocytosis and assess the effect on expression of SIRP-α and SHP-1 in human monocytes. Monocytes were cultured ex vivo with IFN-β or IFN-γ/TNF-α. Erythrophagocytosis was determined by flow cytometry. SIRP-α and SHP-1 gene expression was determined by real time-PCR, while SIRP-α and SHP-1 protein expression was determined by western blot. Erythrophagocytosis by monocytes significantly decreased after treatment with either IFN-β or IFN-γ/TNF-α. Monocytes cultured with IFN-γ/TNF-α showed increased SIRP-α gene and protein expression and SHP-1 gene expression. Monocytes cultured with IFN-β did not show any alteration in SIRP-α or SHP-1 expression. We conclude that IFN-β and IFN-γ/TNF-α decrease erythrophagocytosis by human monocytes in vitro, and this effect does not apparently require an increase in SIRP-α or SHP-1 expression.
Subject: Anemia, Hemolytic, Autoimmune
Antigens, Differentiation
Erythrocyte Membrane
Gene Expression Regulation
Protein Tyrosine Phosphatase, Non-receptor Type 6
Receptors, Immunologic
Tumor Necrosis Factor-alpha
Rights: fechado
Identifier DOI: 10.3109/08923973.2012.697470
Date Issue: 2012
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
File SizeFormat 
pmed_22738830.pdf786.78 kBAdobe PDFView/Open

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