Autoimmunity to the modified self

Hundreds of protein posttranslational modifications (PTMs) have been mapped, greatly expanding the complexity of the cellular proteome and substantially diversifying its functions (1). By changing the protein primary structure, PTMs may change protein function. Additionally, by modifying the self-proteome, PTMs pose a danger for the development of autoimmune diseases because they change the protein “self” sequence. On page 1104 of this issue, Zhai et al. (2) describe how carboxyethylation of integrin αIIb (ITGA2B) is involved in the pathogenesis of the autoimmune disorder, ankylosing spondylitis.