Engagement of MHC-class II molecules by staphylococcal exotoxins delivers a comitogenic signal to human B cells

Ramsay Fuleihan, Walid Mourad, Raif S. Geha, Talal Chatila*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

55 Scopus citations

Abstract

The staphylococcal exotoxin toxic shock syndrome toxin-1 (TSST-1) has been demonstrated to bind to monomorphic determinants on MHC-class II molecules. In this study, we have used TSST-1 to probe the role of MHC-class II molecules in the activation and differentiation of resting human B cells. Highly purified B cells were stimulated with TSST-1, alone or in combination with PMA or with anti-human IgM antibodies (anti-μ) and the resulting B cell proliferation and Ig production were monitored. On its own, TSST-1 failed to induce B cell proliferation or Ig production. However, TSST-1 synergized with PMA and with anti-μ in inducing B cell proliferation in the absence of any added T cells or T cell factors. TSST-1 did not induce or potentiate early activation events associated with anti-μ treatment such as phosphoinositide hydrolysis and Ca2+ mobilization. Also, TSST-1 did not potentiate the capacity of anti-μ to induce the transcription of early activation genes such as c-myc. Finally, in contrast to its capacity to promote mitogen-triggered B cell proliferation, TSST-1 failed to induce the differentiation of B lymphocytes into Ig-secreting cells in the absence of added T cells. These results indicate that TSST-1 delivers a comitogenic signal to B cells via MHC-class II molecules that is distinct from signals delivered via surface μ and further strengthens the role of MHC-class II molecules as signal transducing structures.

Original languageEnglish (US)
Pages (from-to)1661-1666
Number of pages6
JournalJournal of Immunology
Volume146
Issue number5
StatePublished - 1991

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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