Bacterial superantigens induce V beta-specific T cell receptor internalization
Details
Serval ID
serval:BIB_7955FB8AE1E3
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Bacterial superantigens induce V beta-specific T cell receptor internalization
Journal
Molecular Immunology
ISSN
0161-5890
Publication state
Published
Issued date
07/1996
Peer-reviewed
Oui
Volume
33
Number
10
Pages
891-900
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Jul
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Jul
Abstract
Staphylococcal enterotoxins can cause toxic shock syndrome and autoimmune diseases. Circulating T cells from these diseases have a very wide range of expression in particular T cell receptor (TCR) beta chain variable regions (V beta). One possibility for this wide range of TCR V beta expression is that during acute infection with organisms secreting superantigens (SAg) these potent molecules might modulate TCR expression. To test this hypothesis, we investigated the potential effects of SAg on TCR V beta cell surface expression. Peripheral blood mononuclear cells (PBMC) from healthy donors were incubated with staphylococcal SAg. Toxic shock syndrome toxin-1 (TSST-1) induced downregulation of V beta 2 expression, whereas staphylococcal enterotoxin (SE) B induced V beta 3-and V beta 12-specific downregulation. TSST-1 did not interfere with anti-V beta 2 mAb binding. Therefore, this downregulation was not due to steric hindrance of Ab binding by TSST-1. TSST-1 induced V beta 2 downregulation was time-, dose- and temperature-dependent. CD3 expression decreased in parallel with reduction of V beta expression. CD4 and CD8 expression were only slightly decreased. CD2, CD25 and HLA-DR expression were upregulated following TSST-1 stimulation of T cell lines. To investigate the fate of TCR after toxin stimulation, V beta 8+ Jurkat T cells were incubated with SEE which is known to stimulate V beta 8+ T cells, and analysed with fluoresence microscopy, and immunoprecipitation and Western blotting. After SEE stimulation, there was an increase in V beta 8 molecules found in the cytoplasm which correlated with loss of cell surface V beta 8 molecules, suggesting internalization of cell surface V beta 8 molecules was induced by SEE stimulation. Shedding of V beta 8 molecules into the culture supernatant was not detected. These data demonstrate that SAg mediated downregulation of TCR expression occurs primarily as the result of TCR internalization. This downregulation phenomenon may have physiological and pathological consequences in patients infected with Staphylococcus aureus.
Keywords
Antibodies, Monoclonal
Antigens, CD2/metabolism
Antigens, CD3/metabolism
Antigens, CD4/metabolism
Antigens, CD8/metabolism
*Bacterial Toxins
Biotin/metabolism
Blotting, Western
Down-Regulation
Enterotoxins/pharmacology
Flow Cytometry
HLA-DR Antigens/metabolism
Humans
Jurkat Cells
Kinetics
Receptors, Antigen, T-Cell, alpha-beta/*metabolism
Receptors, Interleukin-2/metabolism
Superantigens/*immunology
T-Lymphocytes/*immunology/metabolism
Temperature
Pubmed
Web of science
Create date
20/01/2008 15:23
Last modification date
20/08/2019 14:35