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ALCAM/CD166 adhesive function is regulated by the tetraspanin CD9

Alvaro Gilsanz1, Lorena Sánchez-Martín, María Dolores Gutiérrez-López

  • 1Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Nicolás Cabrera 1, Campus de Cantoblanco, 28049, Madrid, Spain.

Cellular and Molecular Life Sciences : CMLS
|October 12, 2012
PubMed

Insights

Activated Cell Adhesion Molecule (ALCAM) interactions are enhanced by the tetraspanin CD9. This CD9-mediated upregulation of ALCAM function boosts cell adhesion, T cell migration, and proliferation.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Activated Cell Adhesion Molecule (ALCAM/CD166) is an immunoglobulin superfamily member mediating cell adhesion via homophilic (ALCAM-ALCAM) or heterophilic (ALCAM-CD6) interactions.
  • ALCAM plays critical roles in leukocyte extravasation, immune synapse stabilization, T cell activation, and tumor metastasis.
  • The precise mechanisms regulating ALCAM's adhesive capacity remain largely unknown.

Purpose of the Study:

  • To elucidate the regulatory mechanisms governing ALCAM's adhesive function.
  • To investigate the role of tetraspanin CD9 in modulating ALCAM-mediated interactions.

Main Methods:

  • Confocal microscopy for colocalization studies.
  • Biochemical analyses to identify protein complexes.
  • Functional assays to assess cell adhesion, migration, activation, and proliferation.

Main Results:

  • ALCAM directly associates with CD9 and the metalloproteinase ADAM17/TACE on leukocyte surfaces.
  • CD9 significantly upregulates both homophilic and heterophilic ALCAM interactions.
  • CD9 enhances ALCAM-mediated cell adhesion and T cell responses.

Conclusions:

  • CD9 enhances ALCAM function through increased ALCAM clustering and surface expression.
  • Inhibition of ADAM17 activity by CD9 contributes to ALCAM surface expression upregulation.
  • These findings reveal a novel regulatory pathway for ALCAM function with implications for immune responses and cancer.

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