Autoimmunity to the modified self

Description Protein posttranslational modifications can break tolerance to the self-proteome 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.

• Publication year

  2023

• Venue

  Science

• Publication date

  2023-03-17

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1126/science.adg3925PMID 36927028
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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