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Tenascin suppresses CD3-mediated T cell activation

S Hibino1, K Kato, S Kudoh

  • 1Fourth Department of Internal Medicine, Nippon Medical School, Tokyo, Bunkyo-ku, 113-8602, Japan.

Biochemical and Biophysical Research Communications
|September 15, 1998
PubMed

Insights

Tenascin (TN) is an immunosuppressive extracellular matrix protein that inhibits T cell proliferation. It interferes with T cell activation regardless of the costimulatory molecules used.

Area of Science:

  • Immunology
  • Cell Biology
  • Extracellular Matrix Biology

Background:

  • Tenascin (TN) is an extracellular matrix protein known to antagonize fibronectin (FN) actions.
  • TN interferes with FN-dependent cell attachment and activation.

Purpose of the Study:

  • To investigate the inhibitory effect of TN on T cell proliferation.
  • To determine if TN affects T cell activation induced by anti-CD3 antibody with various costimulators in serum-free conditions.

Main Methods:

  • Human T cells were cultured in serum-free conditions.
  • T cell proliferation was induced using immobilized anti-CD3 antibody combined with costimulators like FN, VLA-4/FN, VLA-5/FN, VLA-6/laminin, LFA-1, CD2, and CD28.
  • Phorbol ester stimulation was used as a control.

Main Results:

  • TN completely inhibited T cell activation induced by anti-CD3 plus FN.
  • TN interfered with T cell proliferation costimulated by VLA integrin/ligand interactions (VLA-4/FN, VLA-5/FN, VLA-6/laminin).
  • TN also inhibited T cell activation costimulated by LFA-1, CD2, and CD28, but not by phorbol ester.

Conclusions:

  • Tenascin (TN) inhibits anti-CD3-induced T cell proliferation irrespective of the costimulatory molecules used.
  • TN acts as a generally immunosuppressive extracellular matrix protein.
  • TN potentially interferes with T cell receptor/CD3-mediated T cell activation.

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