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SARS spike protein induces phenotypic conversion of human B cells to macrophage-like cells.

Identifieur interne : 001660 ( PubMed/Corpus ); précédent : 001659; suivant : 001661

SARS spike protein induces phenotypic conversion of human B cells to macrophage-like cells.

Auteurs : Shu-Fen Chiang ; Tze-Yi Lin ; Kuan-Chih Chow ; Shiow-Her Chiou

Source :

RBID : pubmed:20667598

English descriptors

Abstract

Massive aggregations of macrophages are frequently detected in afflicted lungs of patients with severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection. In vitro, ectopic expression of transcription factors, in particular CCAAT/enhancer-binding protein alpha (C/EBPα) and C/EBPβ, can convert B cells into functional macrophages. However, little is known about the specific ligands responsible for such phenotype conversion. Here, we investigated whether spike protein of SARS-CoV can act as a ligand to trigger the conversion of B cells to macrophages. We transduced SARS-CoV spike protein-displayed recombinant baculovirus (SSDRB), vAtEpGS688, into peripheral B cells and B lymphoma cells. Cell surface expression of CD19 or Mac-1 (CD11b) was determined by flow cytometry. SSDRB-mediated changes in gene expression profiles of B lymphoma cells were analyzed by microarray. In this report, we showed that spike protein of SARS virus could induce phenotypic conversion of human B cells, either from peripheral blood or B lymphoma cells, to macrophage-like cells that were steadily losing the B-cell marker CD19 and in turn expressing the macrophage-specific marker Mac-1. Furthermore, we found that SSDRB enhanced the expression of CD86, hypoxia-inducible factor-1α (HIF1α), suppressor of cytokine signaling (SOCS or STAT-induced STAT inhibitor)-3, C/EBPβ, insulin-like growth factor-binding protein 3 (IGFBP3), Krüpple-like factor (KLF)-5, and CD54, without marked influence on C/EBPα or PU.1 expression in transduced cells. Prolonged exposure to hypoxia could also induce macrophage-like conversion of B cells. These macrophage-like cells were defective in phagocytosis of red fluorescent beads. In conclusion, our results suggest that conversion of B cells to macrophage-like cells, similar to a pathophysiological response, could be mediated by a devastating viral ligand, in particular spike protein of SARS virus, or in combination with severe local hypoxia, which is a condition often observed in afflicted lungs of SARS patients.

DOI: 10.1016/j.molimm.2010.06.014
PubMed: 20667598

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pubmed:20667598

Le document en format XML

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<ReferenceList>
<Reference>
<Citation>Eur J Immunol. 1994 Jul;24(7):1544-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">8026517</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Int Rev Immunol. 1998;16(5-6):651-82</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">9646181</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Cell. 1991 Jul 26;66(2):233-43</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">1713127</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Curr Opin Hematol. 2006 Jul;13(4):229-36</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16755218</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Biol Chem. 2006 Jun 30;281(26):17552-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16636063</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Curr Opin Genet Dev. 1998 Oct;8(5):545-51</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">9794826</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Leukemia. 2005 Apr;19(4):580-5</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15703779</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Blood. 2006 Aug 15;108(4):1223-9</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16645168</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Am J Pathol. 1990 Aug;137(2):353-67</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">2167011</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Br J Cancer. 1972 Aug;26(4):239-57</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">4561027</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Cell. 2004 May 28;117(5):663-76</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15163413</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Nat Rev Genet. 2000 Oct;1(1):57-64</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11262875</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Cell. 2006 Aug 25;126(4):755-66</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16923394</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Exp Biol Med (Maywood). 2008 Dec;233(12):1537-45</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">18849546</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Am J Pathol. 1987 Oct;129(1):86-91</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">2821817</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Immunol Lett. 2010 Jan 4;127(2):108-18</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">19874850</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Clin Haematol. 1984 Jun;13(2):329-48</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">6088143</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>EMBO J. 2002 Jul 15;21(14):3770-81</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12110589</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Hum Pathol. 2006 Apr;37(4):381-90</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16564911</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Blood. 2002 Jul 15;100(2):483-90</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12091339</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Clin Oncol. 2005 Jun 20;23(18):4048-56</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15961758</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Oncogene. 2003 Jan 16;22(2):291-7</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12527898</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Biochem Biophys Res Commun. 1995 Nov 13;216(2):540-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">7488145</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Blood. 1994 Dec 15;84(12):4107-15</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">7994028</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Pathol. 2003 Jul;200(3):282-9</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12845623</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Exp Med. 2005 Aug 1;202(3):415-24</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16043521</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>FASEB J. 2006 Nov;20(13):2321-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">17077309</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Immunol. 1996 Oct 15;157(8):3627-34</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">8871663</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Nature. 2000 Mar 9;404(6774):193-7</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10724173</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Pathol. 2004 Jun;203(2):622-30</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15141376</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Clin Oncol. 2005 Aug 20;23(24):5739-45</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16009944</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Clin Diagn Lab Immunol. 2002 Nov;9(6):1169-74</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12414746</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Am J Pathol. 1991 Sep;139(3):475-83</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">1716042</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>FASEB J. 2004 Sep;18(12):1456-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15247143</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>FEBS Lett. 2001 Aug 17;503(2-3):151-7</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11513873</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Perit Dial Int. 2004 Mar-Apr;24(2):139-46</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15119634</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Leukoc Biol. 2007 Nov;82(5):1257-65</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">17675562</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Leukoc Biol. 2003 Nov;74(5):916-22</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12960286</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Nat Cell Biol. 1999 Jul;1(3):E69-71</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10559914</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Am J Clin Pathol. 2004 Apr;121(4):574-80</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15080310</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Hum Pathol. 1994 Aug;25(8):810-4</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">8056422</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Am J Respir Cell Mol Biol. 1996 Apr;14(4):309-15</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">8600933</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Leukemia. 1993 Mar;7(3):435-40</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">8445948</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Clin Oncol. 2005 Oct 20;23(30):7604-13</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16186595</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Am J Respir Cell Mol Biol. 2006 Mar;34(3):264-73</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">16254251</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Lancet. 2003 May 24;361(9371):1773-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12781536</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>J Immunol. 2004 Dec 15;173(12):7602-14</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15585888</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Hum Pathol. 2005 Mar;36(3):303-9</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">15791576</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Exp Hematol. 2002 Feb;30(2):126-34</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11823047</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
<ReferenceList>
<Reference>
<Citation>Am J Clin Pathol. 2000 Jun;113(6):774-81</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10874877</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
</record>

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