IFN-beta, IFN-gamma, and TNF-alpha decrease erythrophagocytosis by human monocytes independent of SIRP-alpha or SHP-1 expression

dc.creatorde Almeida, AC
dc.creatorBarbosa, SM
dc.creatorBarjas-Castro, MDR
dc.creatorOlalla-Saad, ST
dc.creatorCondino-Neto, A
dc.date2012
dc.dateDEC
dc.date2014-07-30T18:00:25Z
dc.date2015-11-26T17:00:48Z
dc.date2014-07-30T18:00:25Z
dc.date2015-11-26T17:00:48Z
dc.date.accessioned2018-03-28T23:48:36Z
dc.date.available2018-03-28T23:48:36Z
dc.identifierImmunopharmacology And Immunotoxicology. Informa Healthcare, v. 34, n. 6, n. 1054, n. 1059, 2012.
dc.identifier0892-3973
dc.identifierWOS:000310314800024
dc.identifier10.3109/08923973.2012.697470
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/69205
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/69205
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1278570
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionBackground: 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-alpha (signal regulatory protein-alpha), 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-alpha and dephosphorylation of specific downstream substrates involved in phagocytosis. SIRP-alpha ligation by CD47 may be inhibited by proinflammatory cytokines. Objectives: The aim of this work was to evaluate the effect of IFN-beta, IFN-gamma, and TNF-alpha on erythrophagocytosis and assess the effect on expression of SIRP-alpha and SHP-1 in human monocytes. Materials and methods: Monocytes were cultured ex vivo with IFN-beta or IFN-gamma/TNF-alpha. Erythrophagocytosis was determined by flow cytometry. SIRP-alpha and SHP-1 gene expression was determined by real time-PCR, while SIRP-alpha and SHP-1 protein expression was determined by western blot. Results: Erythrophagocytosis by monocytes significantly decreased after treatment with either IFN-beta or IFN-gamma/TNF-alpha. Monocytes cultured with IFN-gamma/TNF-alpha showed increased SIRP-alpha gene and protein expression and SHP-1 gene expression. Monocytes cultured with IFN-beta did not show any alteration in SIRP-alpha or SHP-1 expression. Conclusion: We conclude that IFN-beta and IFN-gamma/TNF-alpha decrease erythrophagocytosis by human monocytes in vitro, and this effect does not apparently require an increase in SIRP-alpha or SHP-1 expression.
dc.description34
dc.description6
dc.description1054
dc.description1059
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.languageen
dc.publisherInforma Healthcare
dc.publisherLondon
dc.publisherInglaterra
dc.relationImmunopharmacology And Immunotoxicology
dc.relationImmunopharmacol. Immunotoxicol.
dc.rightsfechado
dc.rightshttp://informahealthcare.com/userimages/ContentEditor/1255620309227/Copyright_And_Permissions.pdf
dc.sourceWeb of Science
dc.subjectErythrophagocytosis
dc.subjectSIRP-alpha
dc.subjectSHP-1
dc.subjectcytokines
dc.subjectphagocytes
dc.subjectTumor-necrosis-factor
dc.subjectInterferon-gamma
dc.subjectNitric-oxide
dc.subjectAutoimmune Encephalomyelitis
dc.subjectMacrophage Activation
dc.subjectBystander Activation
dc.subjectSplenic Macrophages
dc.subjectMolecular Mimicry
dc.subjectViral-infections
dc.subjectStem-cells
dc.titleIFN-beta, IFN-gamma, and TNF-alpha decrease erythrophagocytosis by human monocytes independent of SIRP-alpha or SHP-1 expression
dc.typeArtículos de revistas


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