ReviewImmunological reviews2026
Beta Cell Stress to Epitope Diversification: Post-Translationally Modified Antigens in Type 1 Diabetes.
Review in Immunological reviews, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
0 citing papers in PubMed.
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Authors and funding
3 authors.
Funding
Abstract
Pancreatic beta cells are active participants in the loss of immune tolerance because their high secretory demand creates exceptional vulnerability to inflammatory exposure, endoplasmic reticulum (ER) stress, calcium dysregulation, and redox imbalance. These conditions can promote enzymatic and nonenzymatic changes in self-proteins, generating post-translationally modified (PTM) antigens and neoepitopes that were absent or poorly represented during immune tolerance. This review integrates the contributions with the broader type 1 diabetes (T1D) field to examine how beta cell stress, transglutaminase-2 dependent reactions, peptidyl-arginine deiminase mediated citrullination, oxidative modifications, and post-translational peptide fusion reshape the antigenic landscape. We consider how these products alter antigen presentation and recognition by autoreactive T cells and how an evolving neoepitope repertoire may promote antigenic diversification and epitope spreading. Importantly, clonal recruitment of new determinants must be distinguished from apparent broadening caused by T cell receptor (TCR) cross-reactivity, dual-TCR expression, bystander activation, or tissue redistribution. Defining when modified epitopes arise, which are naturally presented, and which responses contribute to pathogenesis could improve biomarker development, patient stratification, and therapeutic strategies designed to reduce beta cell stress, thus enhancing survival and identity maintenance, while restoring immune tolerance.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.