Upregulation of IgE synthesis by staphylococcal toxic shock syndrome toxin-1 in peripheral blood mononuclear cells from patients with atopic dermatitis
Details
Serval ID
serval:BIB_EB058B9675AA
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Upregulation of IgE synthesis by staphylococcal toxic shock syndrome toxin-1 in peripheral blood mononuclear cells from patients with atopic dermatitis
Journal
Clinical and Experimental Allergy
ISSN
0954-7894
Publication state
Published
Issued date
12/1995
Peer-reviewed
Oui
Volume
25
Number
12
Pages
1218-27
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Dec
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Dec
Abstract
BACKGROUND: Atopic dermatitis (AD) is a chronic skin disease associated with increased IgE synthesis and colonization with Staphylococcus aureus secreting exotoxins, such as Toxic Shock Syndrome Toxin-1 (TSST-1). OBJECTIVES: In this study, we were interested in determining the in vitro effects of TSST-1 on IgE synthesis in peripheral blood mononuclear cells from patients with AD. METHODS: We stimulated peripheral blood mononuclear cells (PBMC) from AD patients with a wide range of TSST-1 concentrations and measured IgE synthesis by enzyme-linked immunosorbent assay (ELISA) after 14 days. RESULTS: We show herein that TSST-1 produced antagonistic effects on IgE synthesis by PBMC from AD patients, depending on the concentration used: IgE synthesis was inhibited at 1000 pg/mL (P < 0.05) and enhanced at 0.01 pg/mL (P < 0.01) of toxin. TSST-1 was found to induce the production of much higher amounts of interferon-gamma (IFN gamma) at 1000 pg/mL than at 0.01 pg/mL of toxin (P = 0.0001). More importantly, immunoglobulin E (IgE) synthesis was enhanced by TSST-1 at 1 pg/mL in the presence of antibodies blocking IFN gamma activity. The other immunoglobulin (Ig) isotypes were also increased after TSST-1 stimulation suggesting that the enhanced IgE synthesis was secondary to a polyclonal B cell activation rather than an isotype switch. TSST-1-stimulated IgE synthesis was T cell-dependent because purified tonsil B cells were only able to synthesize increased amounts of IgE when small numbers of T cells were added to the cultures. Anti-HLA-DR and anti-LFA-1 monoclonal antibodies (MoAb) inhibited TSST-1-enhanced IgE synthesis, suggesting that the bridging of the T cell receptor (TCR) and major histocompatibility complex (MHC) class II on B cells was necessary for activation of B cell differentiation. CONCLUSION: These data indicate that staphylococcal superantigens are able, at concentrations inducing low amounts of IFN gamma, to stimulate IgE synthesis by PBMC from AD patients, and suggest that staphylococcal toxins may contribute to elevated IgE synthesis in AD.
Keywords
Adjuvants, Immunologic/pharmacology
Adult
B-Lymphocytes/immunology
*Bacterial Toxins
Cells, Cultured
Dermatitis, Atopic/blood/*immunology
Enterotoxins/antagonists & inhibitors/immunology/*pharmacology
Humans
Immunoglobulin E/*biosynthesis/drug effects
Interferon Type II/pharmacology
Leukocytes, Mononuclear/drug effects/*immunology
Lymphocyte Activation
Staphylococcus aureus/*immunology
Superantigens/*pharmacology
T-Lymphocytes/immunology
Tonsil/cytology
Up-Regulation/*immunology
Pubmed
Web of science
Create date
20/01/2008 15:22
Last modification date
20/08/2019 16:13