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Related Concept Videos

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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.
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Immunoglobulin-like cell adhesion molecules or Ig-CAMs are a versatile group of cell surface glycoproteins belonging to the immunoglobulin protein superfamily. Ig-CAMs possess the characteristic immunoglobulin protein domains and other domains such as the fibronectin type III domain. The Ig domains are glycosylated to varying degrees in different Ig-CAMs.
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Related Experiment Video

Updated: Mar 17, 2026

Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation
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Inflammatory Th17 Cells Express Integrin αvβ3 for Pathogenic Function.

Fang Du1, Abhishek V Garg1, Karis Kosar1

  • 1Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh, 3500 Terrace Street, Pittsburgh, PA 15261, USA.

Cell Reports
|July 26, 2016
PubMed
Summary
This summary is machine-generated.

Interleukin-23 (IL-23) drives integrin beta3 expression on Th17 cells, crucial for autoimmune inflammation in experimental autoimmune encephalomyelitis (EAE). Blocking integrin beta3 ameliorates EAE, highlighting its role in Th17 cell function.

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Area of Science:

  • Immunology
  • Neuroscience
  • Cell Biology

Background:

  • Interleukin-23 (IL-23) is vital for inflammatory T helper 17 (Th17) cell function in experimental autoimmune encephalomyelitis (EAE).
  • IL-23 blockade reduces effector Th17 cells in the central nervous system (CNS).

Purpose of the Study:

  • To investigate the role of integrin beta3 in Th17 cell function and autoimmune CNS inflammation.
  • To determine if IL-23 regulates integrin beta3 expression on Th17 cells.

Main Methods:

  • Analysis of integrin beta3 expression on T cells in EAE models.
  • Administration of integrin alphaVbeta3 inhibitors.
  • Assessment of EAE induction and progression in integrin beta3-deficient mice.

Main Results:

  • Pro-inflammatory Th17 cells express high levels of IL-23-dependent integrin beta3.
  • Integrin beta3 is upregulated on effector Th17 cells and "ex-Th17" cells, but not all activated T cells.
  • Integrin alphaVbeta3 inhibitors and integrin beta3 deficiency ameliorated EAE clinical signs.
  • Integrin beta3 deficiency on CD4+ T cells blocked EAE induction.
  • Integrin beta3-deficient Th17 cells showed impaired EAE induction, reduced CNS lesion size, and decreased migration.

Conclusions:

  • Integrin beta3 is essential for Th17 cell-mediated autoimmune CNS inflammation.
  • Targeting integrin beta3 may offer a therapeutic strategy for EAE and related autoimmune diseases.