ArticleImmunity, inflammation and disease2023
4-1BB and cytokines trigger human NK, γδ T, and CD8
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Cytokine-induced expandable memory NK cells with significant metabolic, epigenetic remodeling, and persistence properties.Cell death discovery · 2026Article
- Mechanisms of T cell activation: Integrating signaling pathways, experimental models, and therapeutic implications.EXCLI journal · 2026Review
- Secretome and Cellular Composition of Peripheral Blood Mononuclear Cells Cultured in the Presence of Cell Feeder or Interleukins.Bulletin of experimental biology and medicine · 2025Article
- Uncovering the Expression Pattern of the Costimulatory Receptors ICOS, 4-1BB, and OX-40 in Exhausted Peripheral and Tumor-Infiltrating Natural Killer Cells from Patients with Cervical Cancer.International journal of molecular sciences · 2024Article
- 4-1BB and cytokines trigger human NK, γδ T, and CD8Immunity, inflammation and disease · 2023Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThis study was designed to compare the costimulatory molecules and cytokines required to trigger the proliferation and activation of natural killer (NK), γδ T, and CD8
methodsK562-derived artificial antigen-presenting cells (aAPCs); that is, K562 forced to express CD86 and 4-1BBL costimulatory receptors, in the presence of cytokines, were used to mimic dendritic cells (DCs) and provide signals to support the proliferation and activation of NK, γδ T, and CD8
resultsThree signals are required to trigger optimal proliferation in MART-1-specific CD8
conclusionsTherefore, lymphocytes committed to kill are produced as inactive precursors, and the license to kill is delivered by three signals, allowing for extensive proliferation and effector function acquisition. This data challenges the paradigm of anergy and supports the danger signal theory originally proposed by Polly Matzinger, which states that killer cells are tolerant by default, thereby protecting the mammalian body from autoimmunity.
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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.