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http://hdl.handle.net/10261/153913
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dc.contributor.author | Borroto Revuelta, Aldo | - |
dc.contributor.author | Reyes-Garau, Diana | - |
dc.contributor.author | Jiménez, M. Angeles | - |
dc.contributor.author | Carrasco Romero, Esther | - |
dc.contributor.author | Moreno, Beatriz | - |
dc.contributor.author | Martínez-Pasamar, Sara | - |
dc.contributor.author | Cortés, José R. | - |
dc.contributor.author | Perona, Almudena | - |
dc.contributor.author | Abia, David | - |
dc.contributor.author | Blanco, Soledad | - |
dc.contributor.author | Fuentes, Manuel | - |
dc.contributor.author | Arellano Rojo, Irene | - |
dc.contributor.author | Lobo, Juan | - |
dc.contributor.author | Heidarieh, Haleh | - |
dc.contributor.author | Rueda, Javier | - |
dc.contributor.author | Esteve, Pilar | - |
dc.contributor.author | Cibrián, Danay | - |
dc.contributor.author | Martínez-Riaño, Ana | - |
dc.contributor.author | Mendoza, Pilar | - |
dc.contributor.author | Prieto López, Cristina | - |
dc.contributor.author | Calleja, Enrique | - |
dc.contributor.author | Oeste, Clara L. | - |
dc.contributor.author | Orfao, Alberto | - |
dc.contributor.author | Fresno, Manuel | - |
dc.contributor.author | Sánchez-Madrid, Francisco | - |
dc.contributor.author | Alcamí, Antonio | - |
dc.contributor.author | Bovolenta, Paola | - |
dc.contributor.author | Martín, Pilar | - |
dc.contributor.author | Villoslada, Pablo | - |
dc.contributor.author | Morreale, Antonio | - |
dc.contributor.author | Messeguer, Àngel | - |
dc.contributor.author | Alarcón, Balbino | - |
dc.date.accessioned | 2017-08-07T11:08:34Z | - |
dc.date.available | 2017-08-07T11:08:34Z | - |
dc.date.issued | 2016 | - |
dc.identifier | doi: 10.1126/scitranslmed.aaf2140 | - |
dc.identifier | issn: 1946-6242 | - |
dc.identifier.citation | Science Translational Medicine 8 (2016) | - |
dc.identifier.uri | http://hdl.handle.net/10261/153913 | - |
dc.description.abstract | Modulating T cell activation is critical for treating autoimmune diseases but requires avoiding concomitant opportunistic infections. Antigen binding to the T cell receptor (TCR) triggers the recruitment of the cytosolic adaptor protein Nck to a proline-rich sequence in the cytoplasmic tail of the TCR's CD3e subunit. Through virtual screening and using combinatorial chemistry, we have generated an orally available, low-molecular weight inhibitor of the TCR-Nck interaction that selectively inhibits TCR-triggered T cell activationwith an IC50 (median inhibitory concentration) ~1 nM. By modulating TCR signaling, the inhibitor prevented the development of psoriasis and asthma and, furthermore, exerted a long-lasting therapeutic effect in a model of autoimmune encephalomyelitis. However, it did not prevent the generation of a protective memory response against amouse pathogen, suggesting that the compound might not exert its effects through immunosuppression. These results suggest that inhibiting an immediate TCR signal has promise for treating a broad spectrumof human T cell-mediated autoimmune and inflammatory diseases. | - |
dc.rights | closedAccess | - |
dc.title | First-in-class inhibitor of the T cell receptor for the treatment of autoimmune diseases | - |
dc.type | artículo | - |
dc.identifier.doi | 10.1126/scitranslmed.aaf2140 | - |
dc.date.updated | 2017-08-07T11:08:35Z | - |
dc.description.version | Peer Reviewed | - |
dc.language.rfc3066 | eng | - |
dc.relation.csic | Sí | - |
dc.type.coar | http://purl.org/coar/resource_type/c_6501 | es_ES |
item.grantfulltext | none | - |
item.openairetype | artículo | - |
item.cerifentitytype | Publications | - |
item.fulltext | No Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
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