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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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Related Experiment Video

Updated: Mar 6, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
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Targeting Impaired Type I Interferon-IL-27 Signaling Rescues T Regulatory Cell Suppressive Function in

Manal Elzoheiry1,2, Maryam Seyedsadr1,3, John Wrobel4

  • 1Department of Neurology, Thomas Jefferson University, Philadelphia, PA, USA.

Biorxiv : the Preprint Server for Biology
|March 5, 2026
PubMed
Summary
This summary is machine-generated.

Regulatory T cells (Tregs) from relapsing-remitting multiple sclerosis (RRMS) patients show impaired function due to decreased type I IFN and IL-27 signaling. IL-27 stimulation in vitro and in vivo restored Treg function, suggesting therapeutic potential for MS treatment.

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Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
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Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
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Area of Science:

  • Immunology
  • Neuroimmunology
  • Cellular and Molecular Medicine

Background:

  • T regulatory cells (Tregs) are crucial for immune homeostasis.
  • Tregs from relapsing-remitting multiple sclerosis (RRMS) patients exhibit impaired suppressive function.
  • The molecular mechanisms underlying RRMS Treg dysfunction are not fully understood, particularly regarding type I interferon (IFN) and IL-27 signaling pathways.

Purpose of the Study:

  • To investigate the molecular mechanisms of Treg dysfunction in RRMS.
  • To explore the therapeutic potential of targeting IFN and IL-27 signaling pathways to restore Treg function in RRMS.
  • To evaluate the efficacy of cGAMP-loaded microparticles (MPs) in ameliorating experimental autoimmune encephalomyelitis (EAE) by modulating Treg function.

Main Methods:

  • Single-cell RNA sequencing (scRNAseq) of Tregs from RRMS patients and healthy controls (HCs).
  • Treatment of EAE model with cGAMP-MPs to activate the stimulator of IFN genes (STING) pathway.
  • Genetic manipulation using Treg-specific IL-27R knockout mice (Treg ΔIl27ra).
  • In vitro IL-27 stimulation of RRMS-derived Tregs.

Main Results:

  • RRMS Tregs display down-regulation of type I IFN and IL-27 signaling pathways, with reduced expression of IFN-stimulated genes (ISGs) and key Treg suppressive mediators.
  • cGAMP-MP treatment ameliorated EAE by inducing Tregs expressing IL-27R, IL-10, TGF-b, and Granzyme B.
  • The therapeutic effect of cGAMP-MP treatment in EAE was dependent on IL-27 signaling, as it was abolished in Treg ΔIl27ra mice.
  • In vitro IL-27 stimulation restored the expression of IFN pathway genes and Treg suppressive genes in RRMS Tregs.

Conclusions:

  • Decreased type I IFN and IL-27 signaling contribute to Treg dysfunction in RRMS.
  • Activating the STING pathway with cGAMP-MPs can restore Treg suppressive function and ameliorate EAE, highlighting the role of IL-27 signaling.
  • IL-27 pre-stimulation holds promise for restoring Treg suppressive function and enhancing their migration to the central nervous system (CNS) in future clinical applications for RRMS.