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Biomedicines
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New Advances in the Role of Regulatory T Cells in...
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New Advances in the Role of Regulatory T Cells in Immunity

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 498

Special Issue Editor

Dr. Mehdi Benamar

E-Mail Website
Guest Editor
Boston Children's Hospital, Boston, MA, USA
Interests: tolerance; immunology; regulatory T cells; allergy; auto-immunity; infections

Special Issue Information

Dear Colleagues,

Numerous diseases, such as allergies, autoinflammatory conditions, and autoimmune disorders, disrupt immune regulation. This disruption signifies a fundamental breakdown of the mechanisms that normally control excessive immune responses. One critical aspect of this regulation involves regulatory T cells (Treg cells), which are responsible for maintaining immunological tolerance in peripheral tissues towards one’s own antigens, friendly bacteria, and harmless foreign substances.

The objective of this Special Issue is to compile an extensive collection of articles focused on recent advancements in the field of regulatory T cells and their role in immune systems. This Special Issue will encompass a wide spectrum of Treg-related subjects, ranging from fundamental research to translational studies. We eagerly invite submissions of original research articles, and reviews on a broad range of topics including, but not limited to, the following:

  • Cutting-edge developments in regulatory T cells and their function in immunity;
  • Exploring the role of Treg cells in allergic, autoinflammatory, and autoimmune disorders;
  • Translational applications of Treg cell research in clinical settings;
  • Mechanisms of Treg cell-mediated immune response (immunosuppression, tissue repair, and others);
  • Novel therapeutic strategies targeting Treg cells in immune-related diseases.

Dr. Mehdi Benamar
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • regulatory T cells
  • immune regulation
  • autoimmune diseases
  • tolerance
  • Foxp3
  • immunomodulatory therapies

Published Papers (1 paper)

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Research

20 pages, 3412 KiB  
Article
Induction of FoxP3 Pre-mRNA Alternative Splicing to Enhance the Suppressive Activity of Regulatory T Cells from Amyotrophic Lateral Sclerosis Patients
by Dmitry D. Zhdanov, Yulia A. Gladilina, Varvara G. Blinova, Anna A. Abramova, Anastasia N. Shishparenok and Daria D. Eliseeva
Biomedicines 2024, 12(5), 1022; https://doi.org/10.3390/biomedicines12051022 - 7 May 2024
Viewed by 300
Abstract
Forkhead box protein 3 (FoxP3) is a key transcription factor responsible for the development, maturation, and function of regulatory T cells (Tregs). The FoxP3 pre-mRNA is subject to alternative splicing, resulting in the translation of multiple splice variants. We have shown that Tregs [...] Read more.
Forkhead box protein 3 (FoxP3) is a key transcription factor responsible for the development, maturation, and function of regulatory T cells (Tregs). The FoxP3 pre-mRNA is subject to alternative splicing, resulting in the translation of multiple splice variants. We have shown that Tregs from patients with amyotrophic lateral sclerosis (ALS) have reduced expression of full-length (FL) FoxP3, while other truncated splice variants are expressed predominantly. A correlation was observed between the reduced number of Tregs in the peripheral blood of ALS patients, reduced total FoxP3 mRNA, and reduced mRNA of its FL splice variant. Induction of FL FoxP3 was achieved using splice-switching oligonucleotides capable of base pairing with FoxP3 pre-mRNA and selectively modulating the inclusion of exons 2 and 7 in the mature mRNA. Selective expression of FL FoxP3 resulted in the induction of CD127low, CD152, and Helios-positive cells, while the cell markers CD4 and CD25 were not altered. Such Tregs had an increased proliferative activity and a higher frequency of cell divisions per day. The increased suppressive activity of Tregs with the induced FL FoxP3 splice variant was associated with the increased synthesis of the pro-apoptotic granzymes A and B, and perforin, IL-10, and IL-35, which are responsible for contact-independent suppression, and with the increased ability to suppress telomerase in target cells. The upregulation of Treg suppressive and proliferative activity using splice-switching oligonucleotides to induce the predominant expression of the FoxP3 FL variant is a promising approach for regenerative cell therapy in Treg-associated diseases. Full article
(This article belongs to the Special Issue New Advances in the Role of Regulatory T Cells in Immunity)
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