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Related Experiment Videos

Does staphylococcal enterotoxin B bind directly to murine T cells?

W Qasim1, M A Kehoe, J H Robinson

  • 1Department of Immunology, Medical School, University of Newcastle upon Tyne, U.K.

Immunology
|August 1, 1991
PubMed
Summary

Staphylococcal enterotoxin B (SEB) does not directly bind to T-cell receptors (TcR) on murine T cells without antigen-presenting cells (APC). SEB requires MHC class II molecules for T-cell activation, indicating indirect interaction.

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Area of Science:

  • Immunology
  • Cellular Biology
  • Molecular Biology

Background:

  • Staphylococcal enterotoxin B (SEB) is a superantigen known to activate T cells.
  • The precise mechanism of SEB interaction with T cells, particularly direct binding to the T-cell receptor (TcR), remains under investigation.
  • Antigen-presenting cells (APC) are typically involved in T-cell activation by superantigens.

Purpose of the Study:

  • To investigate the direct binding potential of staphylococcal enterotoxin B (SEB) to murine T cells.
  • To determine if SEB can directly interact with the T-cell receptor (TcR) in the absence of antigen-presenting cells (APC).
  • To elucidate the role of MHC class II molecules in SEB-mediated T-cell activation.

Main Methods:

  • Utilized Th1 and Th2 T-cell clones lacking APC to assess early activation events.

Related Experiment Videos

  • Measured intracellular free calcium and inositol phosphate accumulation as indicators of T-cell activation.
  • Performed proliferation assays using SEB-pulsed T-cell clones, APC-independent T-cell clones, and SEB coupled to Sepharose beads.

    • Main Results:

    • Concanavalin A (Con A) successfully induced calcium fluxes and inositol phosphate accumulation in APC-free T-cell clones.
    • SEB failed to induce calcium fluxes or inositol phosphate turnover in Th1 and Th2 T-cell clones without APC.
    • Proliferation assays confirmed that SEB does not stimulate T-cell clones in the absence of APC, even when coupled to beads.

    Conclusions:

    • SEB does not directly bind to the T-cell receptor (TcR) in the absence of antigen-presenting cells (APC).
    • The results strongly suggest that MHC class II molecules are essential for SEB interaction with T cells.
    • SEB-mediated T-cell activation requires the participation of MHC class II molecules, indicating an indirect binding mechanism to the TcR.