ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Nonmalignant clonal expansions of memory CD8+ T cells that arise with age vary in their capacity to mount recall responses to infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Virtual memory cells make a major contribution to the response of aged influenza-naïve mice to influenza virus infection.Immunity & ageing : I & A · 2018Article
- Diverse heterologous primary infections radically alter immunodominance hierarchies and clinical outcomes following H7N9 influenza challenge in mice.PLoS pathogens · 2015Article
- Article
- Aging of the T cell compartment in mice and humans: from no naive expectations to foggy memories.Journal of immunology (Baltimore, Md. : 1950) · 2014Review
- Polymicrobial sepsis alters antigen-dependent and -independent memory CD8 T cell functions.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Aged mice exhibit a severely diminished CD8 T cell response following respiratory syncytial virus infection.Journal of virology · 2013Article
- Truncated form of TGF-βRII, but not its absence, induces memory CD8+ T cell expansion and lymphoproliferative disorder in mice.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Antigen-specific memory regulatory CD4+Foxp3+ T cells control memory responses to influenza virus infection.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Clinical factors influencing phenotype of HCMV-specific CD8+ T cells and HCMV-induced interferon-gamma production after allogeneic stem cells transplantation.Clinical & developmental immunology · 2013Article
- Early dysregulation of the memory CD8+ T cell repertoire leads to compromised immune responses to secondary viral infection in the aged.Immunity & ageing : I & A · 2012Article
- Avidity of influenza-specific memory CD8+ T-cell populations decays over time compromising antiviral immunity.European journal of immunology · 2012Article
- Translational research in immune senescence: assessing the relevance of current models.Seminars in immunology · 2012Review
- The LCMV gp33-specific memory T cell repertoire narrows with age.Immunity & ageing : I & A · 2012Article
- Early priming minimizes the age-related immune compromise of CD8⁺ T cell diversity and function.PLoS pathogens · 2012Article
- Use it or lose it: establishment and persistence of T cell memory.Frontiers in immunology · 2012Article
- An age-specific CD8+ T cell pathway that impairs the effectiveness of strategies to prolong allograft survival.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- The narrowing of the CD8 T cell repertoire in old age.Current opinion in immunology · 2011Review
- The blood of healthy individuals exhibits CD8 T cells with a highly altered TCR Vb repertoire but with an unmodified phenotype.PloS one · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Immune responsiveness declines with age in part due to the development of CD8(+) T cell clonal expansions (TCEs) that can dominate the peripheral T cell pool. Although some TCEs arise due to persistent Ag stimulation from chronic infections, others arise in the apparent absence of chronic infection. We have recently shown that this latter class of TCEs can arise over time from the memory CD8(+) T cell pool established by an acute viral infection. Unlike TCEs driven by chronic infections, these age-related TCEs do not display the phenotypic and in vitro functional characteristics of exhausted cells. However, the rate at which these age-related TCEs develop from the memory CD8(+) T cell pool, as well as their ability to mount a recall response to secondary pathogen challenge in vivo, is not known. In this study, we analyzed large cohorts of mice over time for the development of TCE following Sendai virus infection and found a progressive increase in the appearance of TCEs, such that most mice showed evidence of TCE within the memory T cell pool by 2 y postinfection. Using a dual adoptive transfer approach to address the recall potential of virus-specific TCEs, we also demonstrate that most TCEs examined are poorly responsive to a secondary infection. Therefore, we provide evidence that the development of TCE is a common occurrence due to the progressive dysregulation of the virus-specific memory T cell pool with age, but many TCEs are profoundly defective in their ability to mediate recall responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.