Discussion in 'ME/CFS research news' started by Mattie, Mar 29, 2018.
A critical finding was to show itaconate switched off an over-active immune system in mice.
“It’s well known that macrophages cause inflammation, but we have just found they can be coaxed to make a biochemical called itaconate. This functions as an important brake, or off switch, on the macrophage, cooling the heat of inflammation in a process never before described,” Prof O’Neill said.
Dr Evanna Mills, who with PhD student Dylan Ryan is the joint first author of the work, said: “The macrophage takes the nutrient glucose, whose day job it is to provide energy, and surprisingly turns it into itaconate. This then blocks production of inflammatory factors, and also protects mice from the lethal inflammation that can occur during infection.”"
From the article:
Paper the article is based on is in Nature this week. Note that the research was done on mice:
Itaconate is an anti-inflammatory metabolite that activates Nrf2 via alkylation of KEAP1 Evanna L. Mills et al.
Separate names with a comma.