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Related Experiment Videos

Signaling pathways activated by leukocyte function-associated Ag-1-dependent costimulation.

H T Ni1, M J Deeths, W Li

  • 1Department of Laboratory Medicine and Pathology, Center for Immunology, University of Minnesota, Minneapolis 55455, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|May 5, 1999
PubMed
Summary

LFA-1 binding to ICAM-1 provides costimulation for T cell proliferation by activating signaling pathways similar to CD28, but with distinct sensitivities. This suggests LFA-1 plays a key role in CD8+ T cell activation in various tissues.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Signaling

Background:

  • T cell proliferation is enhanced by LFA-1 binding to ICAM-1, but the exact mechanisms involving adhesion versus costimulatory signaling remain unclear.
  • It is not well understood if LFA-1 ligation generates unique costimulatory signals distinct from T cell receptor (TCR) activation.

Purpose of the Study:

  • To investigate whether LFA-1 ligation generates distinct costimulatory signals compared to TCR activation.
  • To compare the costimulatory effects of ICAM-1 and B7.1 on CD8+ T cell proliferation and signaling pathways.

Main Methods:

  • Utilized purified ligands to study T cell activation.
  • Analyzed the activation of phosphatidylinositol 3-kinase, sphingomyelinase, and c-Jun NH2-terminal kinase (JNK) pathways.

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  • Assessed the differential sensitivity of LFA-1 and CD28 costimulation to phosphatidylinositol 3-kinase inhibitors.

    • Main Results:

    • ICAM-1 and B7.1 provide comparable costimulation for CD8+ T cell proliferation.
    • Both LFA-1 and CD28 ligation up-regulate phosphatidylinositol 3-kinase, sphingomyelinase, and JNK activities.
    • LFA-1-dependent costimulation is inhibited by phosphatidylinositol 3-kinase inhibitors, while CD28-dependent costimulation is not.

    Conclusions:

    • LFA-1 ligation activates signaling pathways overlapping with CD28, distinct from TCR signaling, contributing to T cell proliferation.
    • Differential sensitivity to phosphatidylinositol 3-kinase inhibition highlights unique aspects of LFA-1 and CD28 signaling.
    • The costimulatory capacity of LFA-1 has broad implications for CD8+ cytotoxic T lymphocyte (CTL) activation in diverse cellular environments.