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dc.contributor.authorSanjurjo, Lucía
dc.contributor.authorAran, Gemma
dc.contributor.authorTéllez, Érica
dc.contributor.authorAmézaga, Núria
dc.contributor.authorArmengol, Carolina
dc.contributor.authorPrats Soler, Clara
dc.contributor.authorLópez Codina, Daniel
dc.contributor.authorSarrias, Maria Rosa
dc.contributor.otherUniversitat Politècnica de Catalunya. Departament de Física
dc.date.accessioned2018-04-12T20:34:29Z
dc.date.available2018-04-12T20:34:29Z
dc.date.issued2018-03-12
dc.identifier.citationSanjurjo, L., Aran, G., Téllez, É., Amézaga, N., Armengol, C., Prats, C., Lopez, D., Sarrias, M. CD5L promotes M2 macrophage polarization through autophagy-mediated upregulation of ID3. "Frontiers in Immunology", 12 Març 2018, vol. 9, p. 1-16.
dc.identifier.issn1664-3224
dc.identifier.urihttp://hdl.handle.net/2117/116217
dc.description.abstractCD5L (CD5 molecule-like) is a secreted glycoprotein that controls key mechanisms in inflammatory responses, with involvement in processes such as infection, atherosclerosis, and cancer. In macrophages, CD5L promotes an anti-inflammatory cytokine profile in response to TLR activation. In the present study, we questioned whether CD5L is able to influence human macrophage plasticity, and drive its polarization toward any specific phenotype. We compared CD5L-induced phenotypic and functional changes to those caused by IFN/LPS, IL4, and IL10 in human monocytes. Phenotypic markers were quantified by RT-qPCR and flow cytometry, and a mathematical algorithm was built for their analysis. Moreover, we compared ROS production, phagocytic capacity, and inflammatory responses to LPS. CD5L drove cells toward a polarization similar to that induced by IL10. Furthermore, IL10- and CD5L-treated macrophages showed increased LC3-II content and colocalization with acidic compartments, thereby pointing to the enhancement of autophagy-dependent processes. Accordingly, siRNA targeting ATG7 in THP1 cells blocked CD5L-induced CD163 and Mer tyrosine kinase mRNA and efferocytosis. In these cells, gene expression profiling and validation indicated the upregulation of the transcription factor ID3 by CD5L through ATG7. In agreement, ID3 silencing reversed polarization by CD5L. Our data point to a significant contribution of CD5L-mediated autophagy to the induction of ID3 and provide the first evidence that CD5L drives macrophage polarization.
dc.format.extent16 p.
dc.language.isoeng
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Spain
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es/
dc.subjectÀrees temàtiques de la UPC::Ciències de la salut::Medicina::Anatomia i fisiologia humana
dc.subject.lcshImmunology
dc.subject.otherc D5 l
dc.subject.otherautophagy
dc.subject.othermacrophage polarization
dc.subject.otherscavenger receptor cysteine rich
dc.subject.othermathematical algorithm
dc.subject.otheri D3
dc.subject.otherphagocytosis
dc.subject.otherefferocytosis
dc.titleCD5L promotes M2 macrophage polarization through autophagy-mediated upregulation of ID3
dc.typeArticle
dc.subject.lemacImmunologia
dc.contributor.groupUniversitat Politècnica de Catalunya. BIOCOM-SC - Grup de Biologia Computacional i Sistemes Complexos
dc.identifier.doi10.3389/fimmu.2018.00480
dc.description.peerreviewedPeer Reviewed
dc.relation.publisherversionhttps://www.frontiersin.org/articles/10.3389/fimmu.2018.00480/full#h12
dc.rights.accessOpen Access
drac.iddocument22010579
dc.description.versionPostprint (published version)
upcommons.citation.authorSanjurjo, L., Aran, G., Téllez, É., Amézaga, N., Armengol, C., Prats, C., Lopez, D., Sarrias, M.
upcommons.citation.publishedtrue
upcommons.citation.publicationNameFrontiers in Immunology
upcommons.citation.volume9
upcommons.citation.startingPage1
upcommons.citation.endingPage16
dc.identifier.pmid29593730


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Except where otherwise noted, content on this work is licensed under a Creative Commons license: Attribution-NonCommercial-NoDerivs 3.0 Spain