Disrupting metabolism to treat autoimmunity

See allHide authors and affiliations

Science  27 Apr 2018:
Vol. 360, Issue 6387, pp. 377-378
DOI: 10.1126/science.aat4984

You are currently viewing the summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution


Autoimmune and inflammatory diseases are diverse conditions caused by inappropriate and prolonged activation of immune cells with associated ongoing production of inflammatory mediators that cause tissue damage. In 2013, dimethyl fumarate (DMF), a methyl ester of fumaric acid used to treat psoriasis (an autoimmune skin condition), was approved for the treatment of multiple sclerosis (MS), a demyelinating autoimmune disease (1). Although this drug is now first-line treatment for relapsing remitting MS, its mechanism of action is elusive (1, 2). On page 449 of this issue, Kornberg et al. (3) provide evidence that the beneficial effects of DMF are related to its ability to inhibit glyceraldehyde-3-phosphate dehydrogenase (GAPDH)—a central enzyme in glucose metabolism (glycolysis)—and, in so doing, inhibit the development and function of inflammatory immune cells, highlighting the promise of targeting metabolism to modulate immune responses.