Staphylococcal exotoxins deliver activation signals to human T-cell clones via major histocompatibility complex class II molecules

Details

Serval ID
serval:BIB_33116DE46F19
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Staphylococcal exotoxins deliver activation signals to human T-cell clones via major histocompatibility complex class II molecules
Journal
Proceedings of the National Academy of Sciences of the United States of America
Author(s)
Spertini  F., Spits  H., Geha  R. S.
ISSN
0027-8424 (Print)
Publication state
Published
Issued date
09/1991
Volume
88
Number
17
Pages
7533-7
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Sep 1
Abstract
We investigated whether staphylococcal exotoxins (SEs), in addition to their capacity to induce T-cell activation restricted by the T-cell receptor (TCR) beta-chain variable region, can deliver an activation signal to human T-cell clones through major histocompatibility complex (MHC) class II molecules. Eleven human T-cell clones (9 alpha beta TCR and 2 gamma delta TCR clones) of different antigenic specificities were tested for their capacity to proliferate in response to toxic shock syndrome toxin 1 (TSST-1) and two SEs, SEA and SEB. In the absence of accessory cells, only 4 alpha beta TCR clones were stimulated to proliferate, each by a single SE, and to mobilize intracellular free Ca2+ in response to that SE, events indicative of TCR engagement and, presumably, recognition restricted by the beta-chain variable region. In the presence of accessory cells, each of the 11 T-cell clones was stimulated to proliferate by any one of the three SEs tested. This apparently TCR-unrestricted SE-mediated polyclonal proliferation of T-cell clones occurred in the absence of an increase in intracellular free Ca2+ and was not dependent on the presence of MHC class II expression on accessory cells. In contrast, SE-mediated polyclonal proliferation did not occur in 3 alpha beta TCR clones derived from an MHC class II-deficient patient. Furthermore, all of the three SEs induced the proliferation of 4 natural-killer-cell clones, suggesting that expression of TCR/CD3 complex is not essential for SE-mediated polyclonal proliferation of activated lymphocytes. These results indicate that MHC class II molecules transduce activation signals to human T- and natural-killer-cell clones.
Keywords
*Bacterial Toxins Calcium/metabolism Cell Line Clone Cells DNA Replication/drug effects Enterotoxins/immunology/*pharmacology HLA-D Antigens/*immunology Humans Killer Cells, Natural/immunology Kinetics Lymphocyte Activation/*drug effects Receptors, Antigen, T-Cell/physiology Staphylococcus aureus/immunology *Superantigens T-Lymphocytes/drug effects/*immunology
Pubmed
Web of science
Create date
25/01/2008 15:19
Last modification date
20/08/2019 13:18
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