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Related Experiment Video

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Preparing T Cell Growth Factor from Rat Splenocytes
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ICOS ligand costimulation is required for T-cell encephalitogenicity.

R A Sporici1, R L Beswick, C von Allmen

  • 1Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.

Clinical Immunology (Orlando, Fla.)
|August 22, 2001
PubMed
Summary
This summary is machine-generated.

Blocking the Inducible T-cell Costimulator (ICOS) ligand interaction with ICOS-Ig inhibits T-cell activation and viability, crucial for experimental autoimmune encephalomyelitis (EAE) development and progression.

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Area of Science:

  • Immunology
  • Neuroimmunology
  • T-cell Biology

Background:

  • Inducible T-cell Costimulator (ICOS) and its ligand (ICOSL) are critical for T-cell responses.
  • ICOS-dependent costimulation plays a role in T-cell activation and effector function.

Purpose of the Study:

  • To investigate the role of the ICOS:ICOSL interaction in the activation and encephalitogenic potential of CD4(+) T-cells.
  • To determine the impact of blocking ICOS signaling on T-cell survival, cytokine production, and experimental autoimmune encephalomyelitis (EAE) development.

Main Methods:

  • MBP-reactive transgenic CD4(+) T-cells were activated in vitro in the presence of ICOS-Ig.
  • T-cell transfer experiments were performed to assess EAE induction.
  • Apoptosis markers (BAX/BCL-2 ratio) and cytokine production (IL-2, IFN-gamma, IL-10) were analyzed.
  • ICOS-Ig was administered to mice with established EAE to evaluate therapeutic potential.

Main Results:

  • ICOS-Ig blockade inhibited the ability of T-cells to transfer EAE, despite their entry into the brain.
  • ICOS-Ig treatment increased apoptosis in CD4(+) T-cells, particularly memory cells, indicated by an elevated BAX/BCL-2 mRNA ratio.
  • IL-2 production remained unaffected, suggesting ICOS-ligand independence for IL-2.
  • IFN-gamma and IL-10 production were suppressed by ICOS-Ig.
  • Administration of ICOS-Ig post-EAE onset ameliorated clinical symptoms.

Conclusions:

  • The ICOS:ICOSL pathway provides essential costimulatory signals for encephalitogenic T-cell activation, survival, and effector function, distinct from CD28.
  • Blocking ICOS signaling presents a potential therapeutic strategy for autoimmune diseases like EAE.
  • ICOSL signaling is critical for maintaining the viability and pathogenic potential of autoreactive T-cells.