{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T02:39:59Z","timestamp":1790822399264,"version":"4.1.0"},"reference-count":376,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T00:00:00Z","timestamp":1785369600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T00:00:00Z","timestamp":1785369600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunological Reviews"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Autoimmune responses are often attributed to failed tolerance to self\u2010proteins, yet protein expression alone cannot explain why certain antigens dominate disease, why autoreactivity emerges under stress, or why specific HLA alleles shape risk. This review presents a framework in which autoimmunity arises from posttranslational remodeling of antigen identity. Rather than limiting PTMs to side chain chemistry, we consider how covalent modifications, altered processing, aberrant translation, peptide recombination, and supramolecular assembly expand the repertoire of molecular forms available for immune recognition. Classical PTMs such as citrullination, deamidation, oxidation, glycosylation, phosphorylation, sulfation, and ubiquitin\u2010like remnants can modify proteolysis, HLA binding, and antibody recognition. Noncanonical pathways, including signal peptide processing, ERAP\u2010dependent trimming, defective ribosomal products, cryptic ORFs, proteasome\u2010catalyzed splicing, and hybrid insulin peptides, further demonstrate that the presented antigenome extends beyond annotated proteins. We also propose that aggregation functions as a supramolecular antigenic modification by altering uptake, persistence, protease accessibility, and local reaction chemistry. Examples from rheumatoid arthritis, celiac disease, type 1 diabetes, multiple sclerosis, systemic lupus erythematosus, inflammatory bowel disease, and autoimmune thyroid disease illustrate how these mechanisms converge. Finally, we discuss mass spectrometry and immunopeptidomics strategies for identifying, validating, and functionally interpreting remodeled antigens in autoimmune disease.<\/jats:p>","DOI":"10.1111\/imr.70150","type":"journal-article","created":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T04:33:12Z","timestamp":1785472392000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Beyond Sequence: Posttranslational Remodeling of Antigens in Autoimmunity"],"prefix":"10.1111","volume":"341","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-0210-9340","authenticated-orcid":false,"given":"Cynthiya","family":"Shrestha","sequence":"first","affiliation":[{"name":"Department of Chemistry University of Tennessee  Knoxville TN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-2787-5674","authenticated-orcid":false,"given":"Holly M.","family":"Weisfelder","sequence":"additional","affiliation":[{"name":"Department of Chemistry University of Tennessee  Knoxville TN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1978-4365","authenticated-orcid":false,"given":"Thanh D.","family":"Do","sequence":"additional","affiliation":[{"name":"Department of Chemistry University of Tennessee  Knoxville TN USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,7,30]]},"reference":[{"key":"e_1_2_11_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41587-022-01464-2"},{"key":"e_1_2_11_3_1","doi-asserted-by":"publisher","DOI":"10.1074\/mcp.M116.063800"},{"key":"e_1_2_11_4_1","doi-asserted-by":"publisher","DOI":"10.18632\/oncotarget.16952"},{"key":"e_1_2_11_5_1","doi-asserted-by":"publisher","DOI":"10.1158\/2326-6066.CIR-16-0280"},{"key":"e_1_2_11_6_1","doi-asserted-by":"publisher","DOI":"10.1007\/s00109-009-0526-4"},{"issue":"10","key":"e_1_2_11_7_1","first-page":"3390","article-title":"CTLs Are Targeted to Kill Beta Cells in Patients With Type 1 Diabetes Through Recognition of a Glucose\u2010Regulated Preproinsulin Epitope","volume":"118","author":"Skowera A.","year":"2008","journal-title":"Journal of Clinical Investigation"},{"key":"e_1_2_11_8_1","doi-asserted-by":"publisher","DOI":"10.1002\/1097-0215(20001101)88:3<432::AID-IJC16>3.0.CO;2-9"},{"key":"e_1_2_11_9_1","doi-asserted-by":"publisher","DOI":"10.1111\/imm.13168"},{"key":"e_1_2_11_10_1","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2018.02463"},{"issue":"24","key":"e_1_2_11_11_1","first-page":"4333","article-title":"Functionally Distinct ERAP1 and ERAP2 Are a Hallmark of HLA\u2010A29\u2010(Birdshot) Uveitis","volume":"27","author":"Kuiper J. 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