ArticleBlood2007
Nonmalignant T cells stimulate growth of T-cell lymphoma cells in the presence of bacterial toxins.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 78 citations in OpenAlex.
- Trial
- TCRVβ-targeting antibody-drug conjugates as a novel strategy to eliminate malignant T cells in T cell cancers.Blood advances · 2026Article
- Clinical Implications of the Skin Microbiota in the Therapy of Cutaneous T Cell Lymphoma: A Scoping Review.Dermatology and therapy · 2026Review
- Divergent Evolution of Malignant Subclones Maintains a Balance between Induced Aggressiveness and Intrinsic Drug Resistance in T-cell Cancer.Cancer discovery · 2025Article
- The skin microbiome stratifies patients with cutaneous T cell lymphoma and determines event-free survival.NPJ biofilms and microbiomes · 2024Article
- Article
- Role of Antigenic Stimulation in Cutaneous T-Cell Lymphomas.The Journal of investigative dermatology · 2024Review
- The Complex Role of Infectious Agents in Human Cutaneous T-Cell Lymphoma Pathogenesis: From Candidate Etiological Factors to Potential Therapeutics.Pathogens (Basel, Switzerland) · 2024Review
- Article
- The Skin Microbiome in Cutaneous T-Cell Lymphomas (CTCL)-A Narrative Review.Pathogens (Basel, Switzerland) · 2022Review
- Review
- "Alterations in the Skin Microbiota Are Associated With Symptom Severity in Mycosis Fungoides".Frontiers in cellular and infection microbiology · 2022Article
- Article
- Normal and cancer fibroblasts differentially regulate TWIST1, TOX and cytokine gene expression in cutaneous T-cell lymphoma.BMC cancer · 2021Article
- The immunopathogenesis and immunotherapy of cutaneous T cell lymphoma: Pathways and targets for immune restoration and tumor eradication.Journal of the American Academy of Dermatology · 2021Review
- JAK3 Is Expressed in the Nucleus of Malignant T Cells in Cutaneous T Cell Lymphoma (CTCL).Cancers · 2021Article
- Vitamin D Inhibits IL-22 Production Through a Repressive Vitamin D Response Element in theFrontiers in immunology · 2021Article
- Novel targeted therapies of T cell lymphomas.Journal of hematology & oncology · 2020Review
- Staphylococcus aureus enterotoxins induce FOXP3 in neoplastic T cells in Sézary syndrome.Blood cancer journal · 2020Article
- Cellular Interactions and Inflammation in the Pathogenesis of Cutaneous T-Cell Lymphoma.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Bacterial toxins including staphylococcal enterotoxins (SEs) have been implicated in the pathogenesis of cutaneous T-cell lymphomas (CTCLs). Here, we investigate SE-mediated interactions between nonmalignant T cells and malignant T-cell lines established from skin and blood of CTCL patients. The malignant CTCL cells express MHC class II molecules that are high-affinity receptors for SE. Although treatment with SE has no direct effect on the growth of the malignant CTCL cells, the SE-treated CTCL cells induce vigorous proliferation of the SE-responsive nonmalignant T cells. In turn, the nonmalignant T cells enhance proliferation of the malignant cells in an SE- and MHC class II-dependent manner. Furthermore, SE and, in addition, alloantigen presentation by malignant CTCL cells to irradiated nonmalignant CD4(+) T-cell lines also enhance proliferation of the malignant cells. The growth-promoting effect depends on direct cell-cell contact and soluble factors such as interleukin-2. In conclusion, we demonstrate that SE triggers a bidirectional cross talk between nonmalignant T cells and malignant CTCL cells that promotes growth of the malignant cells. This represents a novel mechanism by which infections with SE-producing bacteria may contribute to pathogenesis of CTCL.
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.