期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 126, 期 10, 页码 3942-3960出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI88546
关键词
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资金
- NIH [AG026518, AI093637, LM008111, LM009254, AI06877, AI066121, T32 AI007405, AI052066]
- Juvenile Diabetes Research Foundation [CDA-2-2007-240]
- Diabetes and Endocrinology Research Center [P30-DK057516]
- American Heart Association [13SDG14510023]
Protective T cell memory is an acquired trait that is contingent upon the preservation of its constituents and therefore vulnerable to the potentially deleterious effects of organismal aging. Here, however, we have found that long-term T cell memory in a natural murine host-pathogen system can substantially improve over time. Comprehensive molecular, phenotypic, and functional profiling of aging antiviral CD8(+) memory T cells (CD8(+) T-M) revealed a pervasive remodeling process that promotes the gradual acquisition of distinct molecular signatures, of increasingly homogeneous phenotypes, and of diversified functionalities that combine to confer a CD8(+) T-M-autonomous capacity for enhanced recall responses and immune protection. Notably, the process of CM8(+) T-M aging is characterized by a progressive harmonization of memory and naive T cell traits, is broadly amenable to experimental acceleration or retardation, and serves as a constitutional component for the rebound model of memory T cell maturation. By casting CM8(+) T-M populations within the temporal framework of their slowly evolving properties, this model establishes a simple ontogenetic perspective on the principal organization of CD8(+) T cell memory that may directly inform the development of improved diagnostic, prophylactic, and therapeutic modalities.
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