ArticleImmunology2010
Interleukin-7 enhances memory CD8(+) T-cell recall responses in health but its activity is impaired in human immunodeficiency virus infection.
Article in Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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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
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Association between the IL7R T244I polymorphism and multiple sclerosis risk: a meta analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2016Pooled it
- A Lower Dose of Infection Generates a Better Long-Term Immune Response against Toxoplasma gondii.ImmunoHorizons · 2023Article
- The Association ofNeuropsychiatric disease and treatment · 2022Article
- IL-7 induces sCD127 release and mCD127 downregulation in human CD8European journal of immunology · 2020Article
- Major influence of CD4 count at the initiation of cART on viral and immunological reservoir constitution in HIV-1 infected patients.Retrovirology · 2016Article
- Generalized Liver- and Blood-Derived CD8+ T-Cell Impairment in Response to Cytokines in Chronic Hepatitis C Virus Infection.PloS one · 2016Article
- Mathematical model reveals how regulating the three phases of T-cell response could counteract immune evasion.Immunology · 2015Article
- The effect of human immunodeficiency virus-1 on monocyte-derived dendritic cell maturation and function.Clinical and experimental immunology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Memory CD8(+) T cells regain function during a recall response, but the requirement of signals in addition to antigen during a secondary immune response is unknown. In this study, the ability of interleukin-7 (IL-7) to enhance memory CD8(+ ) CD45RA(- ) CD127(+) T-cell responses in health and in human immunodeficiency virus (HIV) infection was investigated. CD8(+) T-cell-depleted peripheral blood mononuclear cells (PBMCs) from HIV(-) and untreated HIV(+) donors were pulsed with a cytomegalovirus/Epstein-Barr virus/influenza (CEF) peptide pool, and co-cultured with autologous memory CD8(+) T cells in the presence of IL-7. Cell survival and the function of memory CD8(+) T-cell subsets were then evaluated. Memory CD8(+) T-cell proliferation and interferon-γ (IFN-γ) production was enhanced by the presence of antigen, and the addition of IL-7 further enhanced antigen-induced proliferation. In HIV(+) individuals, the presence of antigen enhanced IFN-γ production to a small degree but did not enhance proliferation. Lastly, IL-7 did not enhance antigen-mediated proliferation of memory CD8(+) T cells from HIV(+) individuals. IL-7 therefore appears to have a role in secondary immune responses and its activity is impaired in memory CD8(+) T cells from HIV(+) individuals. These results further our understanding of the signals involved in secondary immune responses, and provide new insight into the loss of CD8(+) T-cell function in HIV infection.
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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.