--- title: "T regulatory cells: mechanisms and therapeutical advances — source content not available" id: "frontiers-in-immunology-15-editorial-t-regulatory-cells-mechanisms-and-therapeutical-advances" canonical_url: "https://medichelpline.com/clinical-feed/frontiers-in-immunology-15-editorial-t-regulatory-cells-mechanisms-and-therapeutical-advances" content_type: "clinical_feed_article" specialty: "Infectious Disease" source_name: "Frontiers in Immunology" source_url: "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1947694" published_at: "2026-08-07T00:00:00.000Z" evidence_level: "Journal Feed" license: "CC-BY-NC-4.0 / Informational Use" --- # T regulatory cells: mechanisms and therapeutical advances — source content not available ## Provenance & Clinical Metadata - **Canonical URL:** https://medichelpline.com/clinical-feed/frontiers-in-immunology-15-editorial-t-regulatory-cells-mechanisms-and-therapeutical-advances - **Specialty:** [Infectious Disease](https://medichelpline.com/clinical-feed/infectious-disease.md) - **Primary Source:** Frontiers in Immunology - **Source URL:** [Original Journal Publication](https://www.frontiersin.org/articles/10.3389/fimmu.2026.1947694) - **Published At:** 2026-08-07T00:00:00.000Z - **Evidence Rating:** Journal Feed ## Executive GIST (TL;DR) - Source article title: "T regulatory cells: mechanisms and therapeutical advances" published under Frontiers in Immunology. - The provided source text contains site navigation, journal sections, and links but does not include the editorial body, abstract, authorship, or any substantive content of the editorial. - The page excerpts show Frontiers platform navigation (About us, Journals, Submit manuscript, Search, Login) and a repeated listing of journal sections, but no article-specific text such as introduction, summary, or conclusions. - Journal sections present on the page include topics relevant to T cell and microbial immunology such as **T Cell Biology**, **Immunological Tolerance and Regulation**, **Viral Immunology**, **Microbial Immunology**, and **Vaccines and Molecular Therapeutics**. - No experimental data, mechanisms, therapeutic approaches, study outcomes, dates, or author details were reported in the supplied source. All article-level content is missing from the provided body. - To access the full editorial content, users should follow the original Frontiers in Immunology article URL or use the journal search/submit/manuscript links shown on the page. - Because the editorial text is not present in the supplied source, this rewrite does not invent or infer any mechanistic or therapeutic details about **T regulatory cells** and limits statements to what the source explicitly shows. ## Clinical Analysis & Structured Key Points Frontiers | Editorial: T regulatory cells: mechanisms and therapeutical advances EDITORIAL article Front. Immunol. , 07 August 2026 Sec. T Cell Biology Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1947694 Published in Frontiers in Immunology T Cell Biology 7 impact factor 11.3 citescore Part of a Research Topic T Regulatory Cells: Mechanisms and Therapeutical Advances 57k views 18 articles Editor & Reviewers Edited and reviewed by M S Mariolina Salio Outline EDITORIAL article Front. Immunol. , 07 August 2026 Sec. T Cell Biology Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1947694 Editorial: T regulatory cells: mechanisms and therapeutical advances G S Gloria Soldevila 1,2 M A Maria-Luisa Alegre 3 K P Karina Pino-Lagos 4 * 1. Department of Immunology, Biomedical Research Institute, National Autonomous University of Mexico, Mexico City, Mexico 2. National Laboratory of Flow Cytometry, Biomedical Research Institute, National Autonomous University of Mexico, Mexico City, Mexico 3. Department of Medicine, University of Chicago, Chicago, IL, United States 4. Facultad de Medicina, Centro de Investigación e Innovación Biomédica CiiB), Universidad de los Andes, Santiago, Chile See more Article metrics View details Editorial on the Research Topic T regulatory cells: mechanisms and therapeutical advances The assembly of this Research Topic was prompted both by the awarding of the 2025 Nobel Prize to work on FoxP3 + regulatory T cells (Tregs) and by the increasing attention these cells have received in a variety of pathological conditions. In parallel with technological advances, FoxP3 + Treg cellular therapies are under investigation to treat different diseases. Here, we introduce a group of manuscripts that include a Hypothesis & Theory article by Bai et al. exposing evidence to support the main idea that Tregs’ modes of suppression are dependent on TCR signaling strength (discussing antigen specificity and bystander suppression), as well as nine reviews and seven original manuscripts. Review articles discussed a wide range of topics from Treg biology (reviewing miRNAs 2 and metabolic reprogramming 3 ) to Tregs in the context of pathology (autoimmunity 4 , hypoxia 5 , leukemia 6 , wound healing 7 , tissue repair and regeneration 8 and tumor immunity 9 ) to Tregs’ clinical applications 10 . Interestingly, most of articles under Original Research classification cover investigation on human Tregs. In this case, Nirmala et al. reported a comprehensive phenotypic characterization (31 markers by flow cytometry) of human Tregs obtained from different sites (cord-blood, peripheral blood, and thymus) concluding that cord-blood contains the most homogenous Treg pool. Regarding Tregs in the context of disease, Kossack et al. reported an immune monitoring study of COVID-19 patients, which found a correlation between COVID-19 severity, Treg phenotypes, and suppression activity, where severe patients contained Tregs with disrupted function. Wang et al 13 . investigated Tregs from patients with Sjögren’s disease, revealing that Treg numbers are decreased whereas expression of cell death-related molecules and apoptosis are increased in these cells. Continuing with the effort to achieve a good Treg product (suppressive cells with stable function), Alvarez-Salazar et al. and Requejo Cier et al. demonstrated that Tregs exposed to Vitamin C or altered with CRISPR-Cas9 technology to avoid susceptibility to tacrolimus maintained an “untouched” Treg signature, opening new possibilities for their application in the transplantation field. From an experimental standpoint, Moya-Guzmán et al. demonstrated that different Treg subsets (namely, thymic Tregs [tTregs], induced Tregs [iTregs] and Retinoic acid-iTregs [RA-Tregs]) all produced small extracellular vesicles (sEVs) with in vitro suppressive activity. This suppression was at least dependent on death of target cells, with sEVs from tTregs and from RA-Tregs being the most cytotoxic. Last, Beguin et al. described a new protocol to test human Tregs in vivo using a xeno- and allogeneic graft-versus-host disease (GvHD) model, as many human Tregs’ function and permanence can be lost or compromised in vivo . The study shows that infused human Tregs engraft in the animals and display suppressive function that can be tracked over time. Together, these contributions capture the dual character of the current Treg field: a maturing understanding of basic biology from TCR signaling and metabolic reprogramming to the mechanisms of suppression, alongside a concerted push toward the clinic. The emphasis on human Tregs across most of the original research, the attention to product stability under pharmacological and genetic manipulation, and the development of improved in vivo testing models all reflect a shared priority: translating decades of foundational work into reliable therapies. As the 2025 Nobel Prize underscores, the questions first raised about how the immune system tolerates self-remain timely and exciting. We hope this Research Topic helps orient readers to both the open biological questions and the practical challenges that will shape the next phase of Treg research. Statements Author contributions GS: Writing – review & editing, Writing – original draft. MA: Writing – review & editing, Writing – original draft. KP: Writing – review & editing, Writing – original draft. Funding The author(s) declared that financial support was received for this work and/or its publication. Pronace-Salud SECIHTI #302815 and Sectei #4868c25 (GS); NIH R01 AI194499 (M-LA); Fondecyt Regular Grant #1261754 (KP-L). Conflict of interest The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Generative AI statement The author(s) declared that generative AI was not used in the creation of this manuscript. Any alternative text (alt text) provided alongside figures in this article has been generated by Frontiers with the support of artificial intelligence and reasonable efforts have been made to ensure accuracy, including review by the authors wherever possible. If you identify any issues, please contact us. Publisher’s note All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. Summary Keywords autoimmunity , cell therapy , extracellular vesicles , GvHD , leukemia , metabolic reprogramming , miRNA , neurodegenerative diseases Citation Soldevila G, Alegre M-L and Pino-Lagos K (2026) Editorial: T regulatory cells: mechanisms and therapeutical advances . Front. Immunol. 17:1947694. doi: 10.3389/fimmu.2026.1947694 Received 24 July 2026 Revised 31 July 2026 Accepted 03 August 2026 Published 07 August 2026 Volume 17 - 2026 Edited and reviewed by Mariolina Salio , Immunocore, United Kingdom Updates Check for updates Copyright © 2026 Soldevila, Alegre and Pino-Lagos. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. * Correspondence: Karina Pino-Lagos, karina.p.lagos@gmail.com Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher. 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