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Autordc.contributor.authorGonzález Ouna, Luis Gustavo
Autordc.contributor.authorSierra Cristancho, Alfredo José
Autordc.contributor.authorRojas Pérez, Carolina Isabel
Autordc.contributor.authorCafferata Chea, Emilio Alfredo
Autordc.contributor.authorMelgar Rodríguez, Samanta Azucena
Autordc.contributor.authorCárdenas Gutiérrez, Angélica María
Autordc.contributor.authorVernal Astudillo, Rolando Marcelo
Fecha ingresodc.date.accessioned2021-11-10T19:33:08Z
Fecha disponibledc.date.available2021-11-10T19:33:08Z
Fecha de publicacióndc.date.issued2021
Cita de ítemdc.identifier.citationAging and Disease Volume 12, Number 5, August 2021es_ES
Identificadordc.identifier.other10.14336/AD.2021.0110
Identificadordc.identifier.urihttps://repositorio.uchile.cl/handle/2250/182650
Resumendc.description.abstractCellular senescence is a biological process triggered in response to time-accumulated DNA damage, which prioritizes cell survival over cell function. Particularly, senescent T lymphocytes can be generated prematurely during chronic inflammatory diseases regardless of chronological aging. These senescent T lymphocytes are characterized by the loss of CD28 expression, a co-stimulatory receptor that mediates antigen presentation and effective T-cell activation. An increased number of premature senescent CD4+CD28- T lymphocytes has been frequently observed in osteolytic diseases, including rheumatoid arthritis, juvenile idiopathic arthritis, ankylosing spondylitis, osteopenia, osteoporosis, and osteomyelitis. Indeed, CD4+CD28- T lymphocytes produce higher levels of osteoclastogenic molecular mediators directly related to pathologic bone loss, such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-17A, and receptor-activator of nuclear factor kappa B ligand (RANKL), as compared with regular CD4(+)CD28(+) T lymphocytes. In addition, premature senescent CD8(+)CD28(-) T lymphocytes have been negatively associated with bone healing and regeneration by inhibiting osteoblast differentiation and mesenchymal stromal cell survival. Therefore, accumulated evidence supports the role of senescent T lymphocytes in osteoimmunology. Moreover, premature senescence of T-cells seems to be associated with the functional imbalance between the osteolytic T-helper type-17 (Th17) and bone protective T regulatory (Treg) lymphocytes, as well as the phenotypic instability of Treg lymphocytes responsible for its trans-differentiation into RANKL-producing exFoxp3Th17 cells, a key cellular phenomenon directly related to bone loss. Herein, we present a framework for the understanding of the pathogenic characteristics of T lymphocytes with a premature senescent phenotype; and particularly, we revise and discuss their role in the osteoimmunology of osteolytic diseases.es_ES
Patrocinadordc.description.sponsorshipFONDECYT from the Agencia Nacional de Investigacion y Desarrollo (ANID), Chile 1181780 Faculty of Dentistry, Universidad de Chile, Chile Fondecyt from ANID 21190087 21180841es_ES
Idiomadc.language.isoenes_ES
Publicadordc.publisherInternational Society on Aging and Disease, USAes_ES
Tipo de licenciadc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
Link a Licenciadc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
Fuentedc.sourceAging and Diseasees_ES
Palabras clavesdc.subjectSenescencees_ES
Palabras clavesdc.subjectT-lymphocyteses_ES
Palabras clavesdc.subjectCD28es_ES
Palabras clavesdc.subjectRANKLes_ES
Palabras clavesdc.subjectOsteoimmunologyes_ES
Palabras clavesdc.subjectBone losses_ES
Títulodc.titlePremature senescence of T-cells favors bone loss during osteolytic diseases. A new concern in the osteoimmunology arenaes_ES
Tipo de documentodc.typeArtículo de revistaes_ES
dc.description.versiondc.description.versionVersión publicada - versión final del editores_ES
dcterms.accessRightsdcterms.accessRightsAcceso abiertoes_ES
Catalogadoruchile.catalogadorapces_ES
Indizaciónuchile.indexArtículo de publícación WoSes_ES


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Attribution-NonCommercial-NoDerivs 3.0 United States
Excepto si se señala otra cosa, la licencia del ítem se describe como Attribution-NonCommercial-NoDerivs 3.0 United States