Although the precise mechanism of action is incompletely characterized, DMF and its active metabolite, MMF, are thought to exert neuroprotective effects in patients with multiple sclerosis by activating the nuclear erythroid 2-related factor 2 (nuclear factor erythroid-derived 2-like 2; Nrf2) transcriptional pathway.
However, since in autoimmune diseases the immune system is exacerbated and there is a damaging surplus of cytokine production, in the treatment of such diseases cytokine induction needs to be tightly regulated. Recently it has been found that DMF is able to inhibit several pathways linked to toll-like receptors (TLRs). In addition, it has been found that DMF can block a specific group of enzymes called the ubiquitin-conjugating enzymes (E2 enzymes). Ubiquitin is a small regulatory protein found in almost all tissues. The addition of ubiquitins to a certain protein is a cellular mechanism to regulate protein expression and location; the ubiquitination process (addition of ubiquitins) can affect a protein’s degradation, change its cellular location, affect its activity and promote or prevent protein interactions. Furthermore, researchers also discovered two key pathways in human immune system responses, the NFκB and ERK1/2 signaling (downstream of TLR), that are inhibited by DMF and correlate with a loss of pro-inflammatory cytokine production.
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