ReviewCells2024
Defining Human Regulatory T Cells beyond FOXP3: The Need to Combine Phenotype with Function.
Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed.
- The anti-inflammatory potential of nicotinamide (vitamin B3) in JIA: modulating Treg numbers and function with nicotinamide.Arthritis research & therapy · 2026Trial
- Immunophenotyping of Human Regulatory T-Cells from Peripheral Blood Mononuclear Cells.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Comment on Raineri et al. Memory Regulatory T Cells as a Biomarker of Early Type 1 Diabetes.Diabetes · 2026Article
- Review
- CD47 and FOXP3Cancers · 2026Review
- Generation of Regulatory T Cells Against Islet Neoantigen.European journal of immunology · 2026Article
- Hypoxia-induced metabolic and apoptotic reprogramming enhances immunomodulation in Wharton's jelly mesenchymal stem cells.iScience · 2026Article
- Multifaceted regulation of immune cells in radiation-induced pulmonary fibrosis: from mechanistic insights to targeted therapies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- FoxP3+ Cells and PNAd+ Tumour-Associated High Endothelial Venules: Synergistic Prognostic Markers in Oral Tongue Squamous Cell Carcinoma.Head and neck pathology · 2026Article
- CAR Treg therapies for neurodegenerative diseases.iScience · 2026Review
- Erosion of Immune Regulation in Diabetic Kidney Disease.Kidney360 · 2026Article
- Targeting regulatory T cells in glioblastoma: from mechanistic insights to novel immunotherapeutic strategies.Frontiers in immunology · 2026Review
- Regulatory T cells in pregnancy disorders: a multi-dimensional framework for biomarkers and therapeutic strategies.Frontiers in immunology · 2026Review
- Research Progress of Molecular HDrug design, development and therapy · 2026Review
- FOXP3 Stability-Adaptation Paradox: Reshaping Treg-Based Therapies for Intestinal Diseases.International journal of biological sciences · 2026Review
- Abatacept treatment shows a modulating effect on Treg subsets in LRBA-deficient patients.Frontiers in immunology · 2026Article
- Divergent CD27 expression marks the Treg induction trajectory.Frontiers in immunology · 2026Article
- Regulatory T cells in human pregnancy: mechanisms, dysregulation, and therapeutic perspectives.Frontiers in immunology · 2026Review
- Selection and Characterisation of Minor Histocompatibility Antigen-Specific Regulatory T Cells in Fully HLA-Matched Setting for GVHD Therapy.European journal of immunology · 2025Article
- iTr35 cells: a novel immunoregulatory subset involved in bone loss in rheumatoid arthritis and clinical implications.Annals of medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulatory T cells (Tregs) are essential to maintain immune homeostasis by promoting self-tolerance. Reduced Treg numbers or functionality can lead to a loss of tolerance, increasing the risk of developing autoimmune diseases. An overwhelming variety of human Tregs has been described, based on either specific phenotype, tissue compartment, or pathological condition, yet the bulk of the literature only addresses CD25-positive and CD127-negative cells, coined by naturally occurring Tregs (nTregs), most of which express the transcription factor Forkhead box protein 3 (FOXP3). While the discovery of FOXP3 was seminal to understanding the origin and biology of nTregs, there is evidence in humans that not all T cells expressing FOXP3 are regulatory, and that not all Tregs express FOXP3. Namely, the activation of human T cells induces the transient expression of FOXP3, irrespective of whether they are regulatory or inflammatory effectors, while some induced T cells that may be broadly defined as Tregs (e.g., Tr1 cells) typically lack demethylation and do not express FOXP3. Furthermore, it is unknown whether and how many nTregs exist without FOXP3 expression. Several other candidate regulatory molecules, such as GITR, Lag-3, GARP, GPA33, Helios, and Neuropilin, have been identified but subsequently discarded as Treg-specific markers. Multiparametric analyses have uncovered a plethora of Treg phenotypes, and neither single markers nor combinations thereof can define all and only Tregs. To date, only the functional capacity to inhibit immune responses defines a Treg and distinguishes Tregs from inflammatory T cells (Teffs) in humans. This review revisits current knowledge of the Treg universe with respect to their heterogeneity in phenotype and function. We propose that it is unavoidable to characterize human Tregs by their phenotype in combination with their function, since phenotype alone does not unambiguously define Tregs. There is an unmet need to align the expression of specific markers or combinations thereof with a particular suppressive function to coin functional Treg entities and categorize Treg diversity.
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.