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               <dc:title>Transgenic expression of soluble human CD5 enhances experimentally-induced autoimmune and anti-tumoral immune responses</dc:title>
               <dc:creator>Fenutría, Rafael</dc:creator>
               <dc:creator>Martinez, Vanesa Gabriela</dc:creator>
               <dc:creator>Simões, Inês</dc:creator>
               <dc:creator>Postigo, Jorge</dc:creator>
               <dc:creator>Gil, Victor</dc:creator>
               <dc:creator>Martínez-Florensa, Mario</dc:creator>
               <dc:creator>Sintes, Jordi</dc:creator>
               <dc:creator>Naves, Rodrigo</dc:creator>
               <dc:creator>Cashman, Kevin S.</dc:creator>
               <dc:creator>Alberola-Ila, José</dc:creator>
               <dc:creator>Ramos Casals, Manuel</dc:creator>
               <dc:creator>Soldevila, Gloria</dc:creator>
               <dc:creator>Raman, Chander</dc:creator>
               <dc:creator>Merino, Jesús</dc:creator>
               <dc:creator>Merino, Ramón</dc:creator>
               <dc:creator>Engel Rocamora, Pablo</dc:creator>
               <dc:creator>Lozano Soto, Francisco</dc:creator>
               <dc:subject>Cèl·lules B</dc:subject>
               <dc:subject>Cèl·lules T</dc:subject>
               <dc:subject>Limfòcits</dc:subject>
               <dc:subject>Antígens</dc:subject>
               <dc:subject>Melsa</dc:subject>
               <dc:subject>Resposta immunitària</dc:subject>
               <dc:subject>B cells</dc:subject>
               <dc:subject>T cells</dc:subject>
               <dc:subject>Lymphocytes</dc:subject>
               <dc:subject>Antigens</dc:subject>
               <dc:subject>Spleen</dc:subject>
               <dc:subject>Immune response</dc:subject>
               <dc:description>CD5 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 shCD5EμTg 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 anti-tumoral 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>
               <dc:date>2017-07-03T11:23:15Z</dc:date>
               <dc:date>2017-07-03T11:23:15Z</dc:date>
               <dc:date>2014-01-15</dc:date>
               <dc:date>2017-07-03T11:23:15Z</dc:date>
               <dc:type>info:eu-repo/semantics/article</dc:type>
               <dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
               <dc:relation>Reproducció del document publicat a: https://doi.org/10.1371/journal.pone.0084895</dc:relation>
               <dc:relation>PLoS One, 2014, vol. 9, num. 1, p. e84895</dc:relation>
               <dc:relation>https://doi.org/10.1371/journal.pone.0084895</dc:relation>
               <dc:rights>cc-by (c) Fenutría, Rafael et al., 2014</dc:rights>
               <dc:rights>http://creativecommons.org/licenses/by/3.0/es</dc:rights>
               <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
               <dc:publisher>Public Library of Science (PLoS)</dc:publisher>
               <dc:source>Articles publicats en revistes (Biomedicina)</dc:source>
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