ArticleJournal of immunology (Baltimore, Md. : 1950)2013
Increased mammalian target of rapamycin complex 2 signaling promotes age-related decline in CD4 T cell signaling and function.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Immunosenescence: signaling pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2025Review
- The aged microenvironment impairs BCL6 and CD40L induction in CD4Aging cell · 2024Article
- Rapamycin Alleviates 2,4,6-Trinitrobenzene Sulfonic Acid-Induced Colitis through Autophagy Induction and NF-Mediators of inflammation · 2022Article
- Single nucleotide polymorphisms in key aging pathways, and phenotypic markers of frailty are associated with increased odds of hospital admission with COVID-19.The Journal of infection · 2021Article
- Sin1-mediated mTOR signaling in cell growth, metabolism and immune response.National science review · 2019Article
- IL-6 Production by TLR-Activated APC Broadly Enhances Aged Cognate CD4 Helper and B Cell Antibody Responses In Vivo.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Intracellular signalling pathways: targets to reverse immunosenescence.Clinical and experimental immunology · 2017Review
- Deep Proteome Analysis Identifies Age-Related Processes in C. elegans.Cell systems · 2016Article
- Regulation of mTOR activity in Snell dwarf and GH receptor gene-disrupted mice.Endocrinology · 2015Article
- Comparison of rapamycin schedules in mice on high-fat diet.Cell cycle (Georgetown, Tex.) · 2014Article
- Aging is not programmed: genetic pseudo-program is a shadow of developmental growth.Cell cycle (Georgetown, Tex.) · 2013Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
CD4 T cell function declines significantly during aging. Although the mammalian target of rapamycin (TOR) has been implicated in aging, the roles of the TOR complexes (TORC1, TORC2) in the functional declines of CD4 T cells remain unknown. In this study, we demonstrate that aging increases TORC2 signaling in murine CD4 T cells, a change blocked by long-term exposure to rapamycin, suggesting that functional defects may be the result of enhanced TORC2 function. Using overexpression of Rheb to activate TORC1 and Rictor plus Sin1 to augment TORC2 in naive CD4 T cells from young mice, we demonstrated that increased TORC2, but not TORC1, signaling results in aging-associated biochemical changes. Furthermore, elevated TORC2 signaling in naive CD4 T cells from young mice leads to in vivo functional declines. The data presented in this article suggest a novel model in which aging increases TORC2 signaling and leads to CD4 T cell defects in old mice.
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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.