Open main menu
Home
Random
Recent changes
Special pages
Community portal
Preferences
About Wikipedia
Disclaimers
Incubator escapee wiki
Search
User menu
Talk
Dark mode
Contributions
Create account
Log in
Editing
Exotoxin
(section)
Warning:
You are not logged in. Your IP address will be publicly visible if you make any edits. If you
log in
or
create an account
, your edits will be attributed to your username, along with other benefits.
Anti-spam check. Do
not
fill this in!
=== Type I: cell surface-active === Type I toxins bind to a receptor on the cell surface and stimulate intracellular signaling pathways. Two examples are described below. ==== Superantigens ==== [[Superantigens]] are produced by several bacteria. The best-characterized superantigens are those produced by the strains of ''[[Staphylococcus aureus]]'' and ''[[Streptococcus pyogenes]]'' that cause [[toxic shock syndrome]]. Superantigens bridge the [[MHC class II]] protein on [[antigen-presenting cells]] with the [[T-cell receptor]] on the surface of [[T cells]] with a particular VΞ² chain. As a consequence, up to 50% of all T cells are activated, leading to massive secretion of proinflammatory [[cytokines]], which produce the symptoms of toxic shock. ==== Heat-stable enterotoxins ==== Some strains of ''[[E. coli]]'' produce [[heat-stable enterotoxin]]s (ST), which are small peptides that are able to withstand heat treatment at 100 Β°C. Different STs recognize distinct receptors on the cell surface and thereby affect different intracellular signaling pathways. For example, STa [[enterotoxins]] bind and activate membrane-bound guanylate cyclase, which leads to the intracellular accumulation of [[cyclic GMP]] and downstream effects on several signaling pathways. These events lead to the loss of electrolytes and water from intestinal cells.
Edit summary
(Briefly describe your changes)
By publishing changes, you agree to the
Terms of Use
, and you irrevocably agree to release your contribution under the
CC BY-SA 4.0 License
and the
GFDL
. You agree that a hyperlink or URL is sufficient attribution under the Creative Commons license.
Cancel
Editing help
(opens in new window)