Suppression of ferroptosis in M1 macrophages may prolong their pro-inflammatory effects, which is relevant to autoimmune diseases such as multiple sclerosis (MS) and inflammatory bowel disease (IBD) ( Extracellular vesicles (EVs)-encompassing exosomes, microvesicles, retrovirus-like particles, and apoptotic bodies-serve as key intercellular mediators that inhibit ferroptosis through activation of the Nrf2 pathway and subsequent upregulation of the antioxidant gene SLC7A11 ( Lipid peroxidation constitute a pivotal mechanism in ferroptosis, varying across different organs, tissues, and cells ( Lipid reactive oxygen species engage MAPK and NF-B signaling cascades to centrally modulate inflammatory processes, as established by current research ( 4.3 Other immune cells involved in ferroptosis Dendritic Cells (DCs) exert a pivotal function in antigen presentation and immune modulation

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