Show simple item record

Authordc.contributor.authorGonzález Ouna, Luis Gustavo
Authordc.contributor.authorSierra Cristancho, Alfredo José
Authordc.contributor.authorRojas Pérez, Carolina Isabel
Authordc.contributor.authorCafferata Chea, Emilio Alfredo
Authordc.contributor.authorMelgar Rodríguez, Samanta Azucena
Authordc.contributor.authorCárdenas Gutiérrez, Angélica María
Authordc.contributor.authorVernal Astudillo, Rolando Marcelo
Cita de ítemdc.identifier.citationAging and Disease Volume 12, Number 5, August 2021es_ES
Abstractdc.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
Publisherdc.publisherInternational Society on Aging and Disease, USAes_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
Link to Licensedc.rights.uri*
Sourcedc.sourceAging and Diseasees_ES
Keywordsdc.subjectBone losses_ES
Títulodc.titlePremature senescence of T-cells favors bone loss during osteolytic diseases. A new concern in the osteoimmunology arenaes_ES
Document typedc.typeArtículo de revistaes_ES
dc.description.versiondc.description.versionVersión publicada - versión final del editores_ES
dcterms.accessRightsdcterms.accessRightsAcceso abiertoes_ES
Indexationuchile.indexArtículo de publícación WoSes_ES

Files in this item


This item appears in the following Collection(s)

Show simple item record

Attribution-NonCommercial-NoDerivs 3.0 United States
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 United States