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PTM\u2010reactive T cells have been identified across numerous autoimmune diseases and, in several cases, implicated directly as pathogenic drivers. Mechanistically, PTMs promote autoimmunity through two intertwined routes: by altering peptide\u2013MHC and TCR binding to favor recognition of self\u2010epitopes, and by generating neoepitopes in peripheral and\/or inflamed tissues that are absent from the thymus, allowing PTM\u2010reactive T cells to escape central tolerance. This cascade is amplified by inflammatory cytokines, upregulated antigen\u2010processing machinery, disease\u2010associated HLA alleles, and, in some cases, exogenous triggers such as diet. We use three well\u2010characterized examples\u2014citrullination in multiple autoimmune disorders, hybrid insulin peptide (HIP) formation in type 1 diabetes, and gluten deamidation in celiac disease\u2014to illustrate how distinct PTM biology, tissue specificity, and genetic encodability shape the antigenic landscape and dictate feasible discovery strategies. We then review four complementary approaches for identifying PTM\u2010specific T cell responses: mass spectrometry\u2010based proteomics and immunopeptidomics, computational MHC\u2010binding prediction, antigen\u2010directed methods, and high\u2010throughput T cell receptor (TCR)\u2010directed library screening methods. For each, we discuss underlying principles, strengths, and limitations, with particular attention to the challenge posed by non\u2010canonical, PTM\u2010bearing residues. By comparing citrullination, HIPs, and gluten deamidation across these methodologies, we highlight how biochemical alterations, tissue accessibility, and mouse\u2010to\u2010human conservation determine which discovery approach is most tractable. We conclude that while synthetic peptide\u2010based methods remain the standard for validating known epitopes, emerging high\u2010throughput, cell\u2010based platforms are rapidly expanding the accessibility of the PTM antigenic landscape for both known and undiscovered autoimmune epitopes.<\/jats:p>","DOI":"10.1111\/imr.70179","type":"journal-article","created":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T04:16:39Z","timestamp":1790568999000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Discovery of Post\u2010Translationally Modified Epitopes in Autoimmunity: Someone Has to Fish so Everyone Can Eat"],"prefix":"10.1111","volume":"343","author":[{"given":"Sanya","family":"Arshad","sequence":"first","affiliation":[{"name":"Center for Systems Immunology University of Pittsburgh School of Medicine  Pittsburgh Pennsylvania USA"},{"name":"Departments of Immunology and Computational Systems Biology University of Pittsburgh School of Medicine  Pittsburgh Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-0756-0223","authenticated-orcid":false,"given":"Benjamin M.","family":"Cameron","sequence":"additional","affiliation":[{"name":"Center for Systems Immunology University of Pittsburgh School of Medicine  Pittsburgh Pennsylvania USA"},{"name":"Departments of Immunology and Computational Systems Biology University of Pittsburgh School of Medicine  Pittsburgh Pennsylvania USA"},{"name":"Graduate Program in Microbiology and Immunology University of Pittsburgh School of Medicine  Pittsburgh Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7554-7447","authenticated-orcid":false,"given":"Alok V.","family":"Joglekar","sequence":"additional","affiliation":[{"name":"Center for Systems Immunology University of Pittsburgh School of Medicine  Pittsburgh Pennsylvania 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