ReviewSeminars in immunology2013
CD4 CTL: living up to the challenge.
Review in Seminars in immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
75 citing papers in PubMed, 119 citations in OpenAlex.
- Effects of microbiota-directed foods in gnotobiotic animals and undernourished children.Science (New York, N.Y.) · 2019Trial
- Functional, Antigen-Specific Stem Cell Memory (TFrontiers in immunology · 2018Trial
- Reduced Plasmodium Parasite Burden Associates with CD38+ CD4+ T Cells Displaying Cytolytic Potential and Impaired IFN-γ Production.PLoS pathogens · 2016Trial
- Cytomegalovirus Drives the Development of Cytotoxic CD4Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- ZBTB7B inhibits glioma tumorigenicity by upregulating GPR17 and CXCL10.Journal of molecular cell biology · 2026Article
- A distinct subset of stem-cell memory is poised for the cytotoxicity program in CD4Science advances · 2026Article
- Unlocking the Potential of Polysaccharides for the Treatment of Lung Cancer.Anti-cancer agents in medicinal chemistry · 2026Review
- A new immunological paradigm for diseases: the protein-homeostasis-system hypothesis.Frontiers in immunology · 2026Review
- Cytotoxic T Cells: Kill, Memorize, and Mask to Maintain Immune Homeostasis.International journal of molecular sciences · 2025Review
- Single cell-resolved cellular, transcriptional, and epigenetic changes in mouse T cell populations linked to age-associated immune decline.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Role of CD4Journal of translational medicine · 2025Review
- Recent Evidence of the Role of CD4JMA journal · 2025Review
- Repertoire-based mapping and time-tracking of T helper cell subsets in scRNA-Seq.Frontiers in immunology · 2025Article
- Balancing Tumor Immunotherapy and Immune-Related Adverse Events: Unveiling the Key Regulators.International journal of molecular sciences · 2024Review
- Article
- Cytotoxic Tph subset with low B-cell helper functions and its involvement in systemic lupus erythematosus.Communications biology · 2024Article
- Cytotoxic CD4Med (New York, N.Y.) · 2023Article
- Healthy aging-would cytotoxic T lymphocytes stand out?Cell death discovery · 2023Article
- Identification of shared characteristics in tumor-infiltrating T cells across 15 cancers.Molecular therapy. Nucleic acids · 2023Article
- Identification of a unique subset of tissue-resident memory CD4Proceedings of the National Academy of Sciences of the United States of America · 2023Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
During thymic development, thymocytes expressing a T cell receptor consisting of an alpha and beta chain (TCRαβ), commit to either the cytotoxic- or T helper-lineage fate. This lineage dichotomy is controlled by key transcription factors, including the T helper (Th) lineage master regulator, the Th-inducing BTB/POZ domain-containing Kruppel-like zinc-finger transcription factor, ThPOK, (formally cKrox or Zfp67; encoded by Zbtb7b), which suppresses the cytolytic program in major histocompatibility complex (MHC) class II-restricted CD4(+) thymocytes and the Runt related transcription factor 3 (Runx3), which counteracts ThPOK in MHC class I restricted precursor cells and promotes the lineage commitment of CD8αβ(+) cytolytic T lymphocytes (CTL). ThPOK continues to repress the CTL gene program in mature CD4(+) T cells, even as they differentiate into effector Th cell subsets. The Th cell fate however is not fixed and two recent studies showed that mature, antigen-stimulated CD4(+) T cells have the flexibility to terminate the expression of ThPOK and functionally reprogram to cytotoxic effector cells. This unexpected plasticity of CD4(+) T cells results in the post-thymic termination of the Th lineage fate and the functional differentiation of distinct MHC class II-restricted CD4(+) CTL. The recognition of CD4 CTL as a defined separate subset of effector cells and the identification of the mechanisms and factors that drive their reprogramming finally create new opportunities to explore the physiological relevance of these effector cells in vivo and to determine their pivotal roles in both, protective immunity as well as in immune-related pathology.
Indexed as
Identifiers
What OpenQuestion holds
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.