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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

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Development and Functional Characterization of Murine Tolerogenic Dendritic Cells
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Myeloid-Derived Suppressor Cell-Derived Interferon-β Promotes T Follicular Helper Cell Response and Exacerbates Lupus

Ke Rui1, Zixiang Chen1,2, Jun Liu1,2

  • 1Department of Laboratory Medicine, Affiliated Hospital of Jiangsu University, Zhenjiang, China.

Arthritis & Rheumatology (Hoboken, N.J.)
|November 28, 2025
PubMed
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Interferon-beta (IFN-β) promotes T follicular helper (Tfh) cell responses in systemic lupus erythematosus (SLE). This discovery offers new therapeutic targets for SLE treatment.

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Area of Science:

  • Immunology
  • Autoimmunity
  • Molecular Biology

Background:

  • T follicular helper (Tfh) cells play a crucial role in autoimmune diseases like systemic lupus erythematosus (SLE).
  • Identifying specific inflammatory cytokines driving Tfh cell responses in SLE is critical for understanding disease pathogenesis.

Purpose of the Study:

  • To identify inflammatory cytokines involved in driving Tfh cell responses in SLE.
  • To elucidate the mechanism by which IFN-β influences Tfh cell differentiation and SLE progression.

Main Methods:

  • Correlation analysis of circulating Tfh frequencies and IFN-β levels with disease activity in SLE patients.
  • In vivo studies using lupus mice treated with IFN-β or deficient in IFNAR1, including adoptive transfer experiments.
  • In vitro analysis of mouse CD4+ T cells treated with IFN-β to examine Tfh differentiation and signaling pathways.
  • Investigation of IFN-β secretion by myeloid-derived suppressor cells (MDSCs) using biochemical assays.

Main Results:

  • Increased Tfh cells and IFN-I inducible gene signatures correlated with disease activity in SLE patients.
  • IFN-β treatment exacerbated disease progression and enhanced Tfh cell responses in lupus mice.
  • IFNAR1 deficiency attenuated lupus progression and reduced Tfh cell responses.
  • IFN-β promoted Tfh cell differentiation via the IDO-Kyn-AhR axis.
  • MDSCs in lupus patients produced high levels of IFN-β, stimulated by autoantigen activated lymphocyte-derived DNA (ALD-DNA) via the cGAS-STING pathway.

Conclusions:

  • IFN-β plays a novel role in promoting Tfh cell responses during lupus progression.
  • This finding highlights IFN-β as a potential therapeutic target for SLE.