Enhancement of LFA-1-mediated cell adhesion by triggering through CD2 or CD3 on T lymphocytes

Y van Kooyk, P van de Wiel-van Kemenade, P Weder, T W Kuijpers, C G Figdor

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The lymphocyte function-associated molecule LFA-1 (CD11a/CD18) plays a key part in lymphocyte adhesion. Lymphocytes do not adhere spontaneously; activation of protein kinase C (PKC) by phorbol esters, however, gives rise to strong LFA-1-dependent adhesion, indicating that activation of LFA-1 is required to induce cell adhesion. We have now investigated whether the functionally important CD2 and CD3 surface structures on T lymphocytes are involved in the activation of LFA-1. The stimulation of these molecules, which causes activation of PKC, strongly promoted LFA-1-dependent adhesion. Furthermore, we demonstrate by using cells from an LFA-1-deficient patient that this enhanced lymphocyte adhesion is caused by activation of the LFA-1 molecule and not by activation of its ligands. LFA-1 was persistently activated by triggering through CD2 but only transiently by triggering through CD3. We postulate that CD2 and CD3 can differentially regulate the affinity of LFA-1 for its ligands by modulating its molecular conformation through PKC-dependent mechanisms.

Original languageEnglish
Pages (from-to)811-3
Number of pages3
Issue number6251
Publication statusPublished - 14 Dec 1989


  • Antigens, CD/physiology
  • Antigens, Differentiation, T-Lymphocyte/physiology
  • Antigens, Differentiation/physiology
  • CD2 Antigens
  • CD3 Complex
  • Cell Adhesion
  • Cell Adhesion Molecules/physiology
  • Cells, Cultured
  • Humans
  • Immunologic Techniques
  • In Vitro Techniques
  • Lymphocyte Function-Associated Antigen-1
  • Protein Kinase C/physiology
  • Receptors, Antigen, T-Cell/physiology
  • Receptors, Immunologic/physiology
  • Receptors, Leukocyte-Adhesion/physiology
  • Signal Transduction
  • T-Lymphocytes/physiology

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