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dc.contributor.authorFenutria, Rafael-
dc.contributor.authorMartínez, Vanesa G.-
dc.contributor.authorPostigo, Jorge-
dc.contributor.authorMerino, Jesús-
dc.contributor.authorMerino, Ramón-
dc.contributor.authorLozano, Francisco-
dc.identifierdoi: 10.1371/journal.pone.0084895-
dc.identifierissn: 1932-6203-
dc.identifier.citationPLoS ONE 9(1): e84895 (2014)-
dc.descriptionThis is an open-access article distributed under the terms of the Creative Commons Attribution License.-- et al.-
dc.description.abstractCD5 is a lymphoid-specific transmembrane glycoprotein constitutively expressed on thymocytes and mature T and B1a lymphocytes. Current data support the view that CD5 is a negative regulator of antigen-specific receptor-mediated signaling in these cells, and that this would likely be achieved through interaction with CD5 ligand/s (CD5L) of still undefined nature expressed on immune or accessory cells. To determine the functional consequence of loss of CD5/CD5L interaction in vivo, a new transgenic mouse line was generated (shCD5EμTg), expressing a circulating soluble form of human CD5 (shCD5) as a decoy to impair membrane-bound CD5 function. These shCD5EmTg mice showed an enhanced response to autologous antigens, as deduced from the presentation of more severe forms of experimentally inducible autoimmune disease (collagen-induced arthritis, CIA; and experimental autoimmune encephalitis, EAE), as well as an increased antitumoral response in non-orthotopic cancer models (B16 melanoma). This enhancement of the immune response was in agreement with the finding of significantly reduced proportions of spleen and lymph node Treg cells (CD4+CD25+FoxP3+), and of peritoneal IL-10-producing and CD5+ B cells, as well as an increased proportion of spleen NKT cells in shCD5EμTg mice. Similar changes in lymphocyte subpopulations were observed in wild-type mice following repeated administration of exogenous recombinant shCD5 protein. These data reveal the relevant role played by CD5/CD5L interactions on the homeostasis of some functionally relevant lymphocyte subpopulations and the modulation of immune responses to autologous antigens.-
dc.description.sponsorshipThis study was supported by grants from the Spanish Ministerio de Economía y Competitividad [Plan Nacional de I+D+i, SAF2010-19717], Generalitat de Catalunya [2009SGR1101], and Instituto de Salud Carlos III [Spanish Network for Research in Infectious Diseases, REIPI RD12/0015/0018] to FL, from Spanish Ministerio de Economía y Competitividad [SAF2011-22463], co-funded by the European Regional Development Fund, to RM, from Ministerio de Economía y Competitividad [SAF2012-34059], co-funded by the European Regional Development Fund, and the Spanish Ministerio de Economía y Competitividad (IPT2011-1527-010000) associated to Fibrostatin SL, to JM, and from NIH AI1076562 and National Multiple Sclerosis Society RG3891 to CR. MM-F and VGM are recipients of fellowships from Agència de Gestió d’Ajuts Universitaris i de Recerca (AGAUR) of the Generalitat de Catalunya [2010TEM37] and from Spanish Ministerio de Economía y Competitividad [JCI-2010-06378], respectively.-
dc.publisherPublic Library of Science-
dc.relation.isversionofPublisher's version-
dc.titleTransgenic expression of soluble human CD5 enhances experimentally-induced autoimmune and anti-tumoral immune responses-
dc.description.versionPeer Reviewed-
dc.contributor.funderMinisterio de Economía y Competitividad (España)-
dc.contributor.funderGeneralitat de Catalunya-
dc.contributor.funderRed Española de Investigación en Patología Infecciosa-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderEuropean Commission-
dc.contributor.funderNational Institutes of Health (US)-
dc.contributor.funderNational Multiple Sclerosis Society (US)-
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