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dc.contributor.author | Minato, Nagahiro | en |
dc.contributor.author | Hattori, Masakazu | en |
dc.contributor.author | Hamazaki, Yoko | en |
dc.contributor.alternative | 湊, 長博 | ja |
dc.contributor.alternative | 濵﨑, 洋子 | ja |
dc.date.accessioned | 2020-12-07T07:54:12Z | - |
dc.date.available | 2020-12-07T07:54:12Z | - |
dc.date.issued | 2020-04 | - |
dc.identifier.issn | 1460-2377 | - |
dc.identifier.uri | http://hdl.handle.net/2433/259424 | - |
dc.description.abstract | Acquired immune function shows recognizable changes over time with organismal aging. These changes include T-cell dysfunction, which may underlie diminished resistance to infection and possibly various chronic age-associated diseases in the elderly. T-cell dysfunction may occur at distinct stages, from naive cells to the end stages of differentiation during immune responses. The thymus, which generates naive T cells, shows unusually early involution resulting in progressive reduction of T-cell output after adolescence, but peripheral T-cell numbers are maintained through antigen-independent homeostatic proliferation of naive T cells driven by the major histocompatibility complex associated with self-peptides and homeostatic cytokines, retaining the diverse repertoire. However, extensive homeostatic proliferation may lead to the emergence of dysfunctional CD4+ T cells with features resembling senescent cells, termed senescence-associated T (SA-T) cells, which increase and accumulate with age. In situations such as chronic viral infection, T-cell dysfunction may also develop via persistent antigen stimulation, termed exhaustion, preventing possible immunopathology due to excessive immune responses. Exhausted T cells are developed through the effects of checkpoint receptors such as PD-1 and may be reversed with the receptor blockade. Of note, although defective in their regular T-cell antigen-receptor-mediated proliferation, SA-T cells secrete abundant pro-inflammatory factors such as osteopontin, reminiscent of an SA-secretory phenotype. A series of experiments in mouse models indicated that SA-T cells are involved in systemic autoimmunity as well as chronic tissue inflammation following tissue stresses. In this review, we discuss the physiological aspects of T-cell dysfunction associated with aging and its potential pathological involvement in age-associated diseases and possibly cancer. | en |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Oxford University Press (OUP) | en |
dc.rights | © The Author(s) 2020. Published by Oxford University Press on behalf of The Japanese Society for Immunology. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com | en |
dc.subject | age-associated diseases | en |
dc.subject | homeostatic proliferation | en |
dc.subject | senescence-associated T cells | en |
dc.subject | T-cell dysfunction | en |
dc.subject | T-cell exhaustion | en |
dc.title | Physiology and pathology of T-cell aging | en |
dc.type | journal article | - |
dc.type.niitype | Journal Article | - |
dc.identifier.jtitle | International immunology | en |
dc.identifier.volume | 32 | - |
dc.identifier.issue | 4 | - |
dc.identifier.spage | 223 | - |
dc.identifier.epage | 231 | - |
dc.relation.doi | 10.1093/intimm/dxaa006 | - |
dc.textversion | publisher | - |
dc.identifier.pmid | 31967307 | - |
dcterms.accessRights | open access | - |
出現コレクション: | 学術雑誌掲載論文等 |
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