ArticleImmunity2020
Endocrine Autoimmune Disease as a Fragility of Immune Surveillance against Hypersecreting Mutants.
Article in Immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Insights into the Genetic and Epigenetic Landscape of Endocrine Autoimmunity: A Systematic Review.Genes · 2025Pooled it
- Article
- Novel perspectives on extracellular vesicles in autoimmune diseases: immunogenicity, inflammation, and immune surveillance.The Journal of clinical investigation · 2026Review
- ERAP1 Allotypes 2 and 10 Differentially Regulate the Immunopeptidome of Melanocytes.Immunology · 2026Article
- Murine T-cell receptor OT-I exhibits imperfect discrimination between foreign and self-antigens.The EMBO journal · 2026Article
- Unifying regulatory motifs in endocrine circuits.Nature communications · 2025Article
- Explosive cytotoxicity of 'ruptoblasts' bridges hormonal surveillance and immune defense.bioRxiv : the preprint server for biology · 2025Article
- An amphiregulin reporter mouse enables transcriptional and clonal expansion analysis of reparative lung Tregs.JCI insight · 2025Article
- Local Enrichment with Convergence of Enriched T-Cell Clones Are Hallmarks of Effective Peptide Vaccination against B16 Melanoma.Vaccines · 2024Article
- Article
- Inflammatory and Infectious Disorders in Endocrine Pathology.Endocrine pathology · 2023Review
- Clonally expanded CD38Science immunology · 2023Article
- EULAR study group on 'MHC-I-opathy': identifying disease-overarching mechanisms across disciplines and borders.Annals of the rheumatic diseases · 2023Review
- Microbiota-dependent proteolysis of gluten subverts diet-mediated protection against type 1 diabetes.Cell host & microbe · 2023Article
- Article
- The β-Cell in Type 1 Diabetes Pathogenesis: A Victim of Circumstances or an Instigator of Tragic Events?Diabetes · 2022Review
- Dynamics of thyroid diseases and thyroid-axis gland masses.Molecular systems biology · 2022Article
- Dynamic follow-up of the effects of programmed death 1 inhibitor treatment on thyroid function and sonographic features in patients with hepatocellular carcinoma.Endocrine connections · 2022Article
- Activation pathways that drive CD4Immunological reviews · 2022Review
- The discriminatory power of the T cell receptor.eLife · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Some endocrine organs are frequent targets of autoimmune attack. Here, we addressed the origin of autoimmune disease from the viewpoint of feedback control. Endocrine tissues maintain mass through feedback loops that balance cell proliferation and removal according to hormone-driven regulatory signals. We hypothesized the existence of a dedicated mechanism that detects and removes mutant cells that missense the signal and therefore hyperproliferate and hypersecrete with potential to disrupt organismal homeostasis. In this mechanism, hypersecreting cells are preferentially eliminated by autoreactive T cells at the cost of a fragility to autoimmune disease. The "autoimmune surveillance of hypersecreting mutants" (ASHM) hypothesis predicts the presence of autoreactive T cells in healthy individuals and the nature of self-antigens as peptides from hormone secretion pathway. It explains why some tissues get prevalent autoimmune disease, whereas others do not and instead show prevalent mutant-expansion disease (e.g., hyperparathyroidism). The ASHM hypothesis is testable, and we discuss experimental follow-up.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.