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Modulation of CD6 function through interaction with Galectin-1 and -3.

Cristina Escoda-Ferran1, Esther Carrasco1, Miguel Caballero-Baños2

  • 1From Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centre Esther Koplowitz, 08036 Barcelona, Spain.

FEBS Letters
|June 20, 2014
PubMed
Summary
This summary is machine-generated.

Galectin-1 and -3 interact with CD6 and CD166/ALCAM, affecting T cell responses. CD6 expression offers protection against galectin-induced cell death, suggesting a role in T cell physiology modulation.

Keywords:
ALCAM/CD166ApoptosisCD6Cell adhesionGalectinT-cell activation

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Area of Science:

  • Immunology
  • Cell Biology
  • Glycobiology

Background:

  • CD6 is a lymphocyte receptor crucial for T cell activation, interacting with CD166/ALCAM at the immunological synapse.
  • Galectins, such as Galectin-1 and -3, are soluble lectins involved in various cellular processes, including immune cell interactions.

Purpose of the Study:

  • To investigate the carbohydrate-dependent interactions between CD6/CD166 and Galectin-1/-3.
  • To determine the functional consequences of these interactions on T cell proliferation, adhesion, and apoptosis.

Main Methods:

  • Carbohydrate-binding assays to study galectin interactions.
  • Functional assays measuring T cell proliferation and adhesion.
  • Flow cytometry to assess galectin-induced apoptosis and CD6 expression.

Main Results:

  • Galectin-1 and -3 bind to CD6 and CD166/ALCAM in a carbohydrate-dependent manner.
  • Galectins inhibit superantigen-induced T cell proliferation and CD6-mediated cell adhesion.
  • CD6 expression confers resistance to galectin-induced apoptosis.

Conclusions:

  • Galectin-1 and -3 interactions with CD6 and CD166/ALCAM modulate T cell proliferation and adhesion.
  • CD6 plays a protective role against galectin-induced T cell apoptosis.
  • These findings suggest a significant role for galectin-CD6/CD166 interactions in regulating T cell physiology.