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Related Experiment Videos

Selective induction of CD8+ cytotoxic T lymphocyte effector function by staphylococcus enterotoxin B

C L Fuller1, V L Braciale

  • 1Department of Microbiology, Beirne B. Carter Center for Immunology Research, Health Sciences Center, University of Virginia, Charlottesville 22908, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|November 20, 1998
PubMed
Summary

Superantigen staphylococcus enterotoxin B (SEB) and influenza peptide both activate CD8+ cytotoxic T lymphocytes (CTLs), but SEB primarily uses FasL/Fas (CD95L/CD95) for cell killing, unlike influenza peptide.

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Ca2+ signaling modulates cytolytic T lymphocyte effector functions.

The Journal of experimental medicine·1998

Area of Science:

  • Immunology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Cytotoxic T lymphocytes (CTLs) are crucial for controlling viral infections by lysing infected cells.
  • Superantigens are potent immune stimulants that induce T cell proliferation and cytokine release.
  • Understanding CTL activation pathways is vital for developing effective immunotherapies.

Purpose of the Study:

  • To compare the activation and cytotoxic mechanisms of CD8+ CTL clones stimulated by influenza peptide/MHC versus the superantigen staphylococcus enterotoxin B (SEB).
  • To investigate the role of intracellular calcium (Ca2+) flux in CTL activation by different stimuli.
  • To determine the primary cytolytic pathway utilized by superantigen-activated CTLs.

Main Methods:

  • Activation of murine influenza-specific CD8+ CTL clones using influenza peptide/MHC and SEB.

Related Experiment Videos

  • Measurement of T cell proliferation and interferon-gamma (IFN-gamma) production.
  • Analysis of cytotoxic mechanisms including perforin, Fas ligand (FasL)/Fas (CD95L/CD95), and serine esterase release.
  • Assessment of intracellular Ca2+ mobilization.

    • Main Results:

    • Both influenza peptide/MHC and SEB induced T cell proliferation and IFN-gamma production.
    • Influenza peptide/MHC triggered both perforin- and FasL/Fas-mediated cytotoxicity.
    • SEB failed to induce perforin-mediated killing or significant intracellular Ca2+ flux, relying mainly on FasL/Fas.
    • SEB induced only a minimal increase in intracellular Ca2+ levels.

    Conclusions:

    • Superantigen-activated CD8+ CTLs exhibit restricted short-term cytolytic potential, primarily mediated through the FasL/Fas (CD95L/CD95) pathway.
    • The distinct intracellular Ca2+ mobilization patterns suggest different activation signaling cascades for peptide versus superantigen stimulation.
    • These findings highlight differential CTL activation pathways with implications for immune response modulation.