Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (662 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by autoimmune diseases.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Autoimmunities; Autoimmune Response; Autoimmune Responses.
Where it fits in the MeSH classification
- Broader topics
- Immunity
- See also
- Autoantibodies; Autoimmune Diseases
Related concepts
Research landscape
PubMed indexes 22,315 records tagged with the MeSH heading “Autoimmunity” (counts retrieved 2026-10-29). 4,852 of them (21.7%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 8,508 records.
Reviews account for 9,573 records (42.9%) and meta-analyses for 83. Randomized controlled trials number 80 (0.4%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 3,231 |
| 2000-2009 | 5,724 |
| 2010-2019 | 8,508 |
| 2020 onward | 4,852 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 9,573 | 42.9% |
| Meta-analyses | 83 | 0.4% |
| Randomized controlled trials | 80 | 0.4% |
Method: PubMed query "Autoimmunity"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in immunology
Immune responses are studied in model organisms, in cells from donors and in patients, and the same pathway can behave differently across these settings. Mouse immune systems differ from human ones in important ways, and blood measurements may not reflect what happens in tissues. Clinical conclusions about immune-mediated disease or immunotherapy come mainly from controlled trials and long-term cohorts. Check the species and tissue studied, whether markers were linked to outcomes patients notice, and the follow-up time.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| CAR-T cell therapy: developments, challenges and expanded applications from cancer to autoimmunity | 2024 | Review article Design not recorded in structured metadata | 76 | cc by PMID 39850899 · DOI · PMC11754230 |
| Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation | 2025 | Review article Design not recorded in structured metadata | 63 | cc by PMID 41155288 · DOI · PMC12563903 |
| Differential roles of human CD4+ and CD8+ regulatory T cells in controlling self-reactive immune responses | 2025 | Research article Design not recorded in structured metadata | 47 | cc by PMID 39806065 · DOI · PMC11785521 |
| 2'-O-Methyl-guanosine RNA fragments antagonize TLR7 and TLR8 to limit autoimmunity | 2026 | Research article Design not recorded in structured metadata | 10 | cc by PMID 41667621 · DOI · PMC13043311 |
CAR-T cell therapy: developments, challenges and expanded applications from cancer to autoimmunity [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Chimeric Antigen Receptor (CAR)-T cell therapy has rapidly emerged as a groundbreaking approach in cancer treatment, particularly for hematologic malignancies.
- Closing excerpt
- By highlighting these cutting-edge developments, this review underscores the transformative potential of CAR technologies in clinical practice.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (120 words)
Chimeric Antigen Receptor (CAR)-T cell therapy has rapidly emerged as a groundbreaking approach in cancer treatment, particularly for hematologic malignancies. However, the application of CAR-T cell therapy in solid tumors remains challenging. This review summarized the development of CAR-T technologies, emphasized the challenges and solutions in CAR-T cell therapy for solid tumors. Also, key innovations were discussed including specialized CAR-T, combination therapies and the novel use of CAR-Treg, CAR-NK and CAR-M cells. Besides, CAR-based cell therapy have extended its reach beyond oncology to autoimmune disorders. We reviewed preclinical experiments and clinical trials involving CAR-T, Car-Treg and CAAR-T cell therapies in various autoimmune diseases. By highlighting these cutting-edge developments, this review underscores the transformative potential of CAR technologies in clinical practice.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39850899 · DOI · PMC11754230
Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Autoimmune diseases are chronic inflammatory conditions characterized by the breakdown of immune tolerance to self-antigens.
- Closing excerpt
- Future research should focus on multi-omics and longitudinal approaches to clarify the reversibility of HPA alterations and identify resilience factors.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (228 words)
Autoimmune diseases are chronic inflammatory conditions characterized by the breakdown of immune tolerance to self-antigens. While genetic and environmental factors play key roles, growing evidence highlights chronic stress as a significant contributor to immune dysregulation through its impact on the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis, primarily via cortisol secretion, serves as the major neuroendocrine mediator of stress responses, influencing both immune regulation and systemic homeostasis. This review synthesizes current literature on HPA axis physiology, the mechanisms of cortisol signaling, and the maladaptive effects of chronic stress. Emphasis is placed on clinical and experimental findings linking HPA dysfunction to immune imbalance and autoimmunity, as well as organ-specific consequences across neuroimmune, endocrine, cardiovascular, gastrointestinal, integumentary, and musculoskeletal systems. Chronic stress leads to impaired HPA axis feedback, glucocorticoid receptor resistance, and paradoxical cortisol dysregulation, fostering a pro-inflammatory state. This dysregulation promotes cytokine imbalance, weakens protective immune mechanisms, and shifts the immune response toward autoimmunity. Evidence from both human and animal studies associates persistent HPA dysfunction with diseases such as systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis. HPA axis dysregulation under chronic stress constitutes a critical mechanistic link between psychological stress and autoimmune disease. Understanding these pathways provides opportunities for therapeutic interventions, including stress management, lifestyle modification, and neuroendocrine-targeted treatments. Future research should focus on multi-omics and longitudinal approaches to clarify the reversibility of HPA alterations and identify resilience factors.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41155288 · DOI · PMC12563903
Differential roles of human CD4+ and CD8+ regulatory T cells in controlling self-reactive immune responses [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Here we analyzed the relative contributions of CD4+ regulatory T cells expressing Forkhead box protein P3 (FOXP3) and CD8+ regulatory T cells expressing killer cell immunoglobulin-like receptors to the control of autoreactive T and B lymphocytes in human tonsil-derived immune organoids.
- Closing excerpt
- These findings highlight the distinct yet complementary roles of CD8+ and CD4+ regulatory T cells in regulating cellular and humoral responses to prevent autoimmunity.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (168 words)
Here we analyzed the relative contributions of CD4+ regulatory T cells expressing Forkhead box protein P3 (FOXP3) and CD8+ regulatory T cells expressing killer cell immunoglobulin-like receptors to the control of autoreactive T and B lymphocytes in human tonsil-derived immune organoids. FOXP3 and GZMB respectively encode proteins FOXP3 and granzyme B, which are critical to the suppressive functions of CD4+ and CD8+ regulatory T cells. Using CRISPR-Cas9 gene editing, we were able to achieve a reduction of ~90-95% in the expression of these genes. FOXP3 knockout in tonsil T cells led to production of antibodies against a variety of autoantigens and increased the affinity of influenza-specific antibodies. By contrast, GZMB knockout resulted in an increase in follicular helper T cells, consistent with the ablation of CD8+ regulatory T cells observed in mouse models, and a marked expansion of autoreactive CD8+ and CD4+ T cells. These findings highlight the distinct yet complementary roles of CD8+ and CD4+ regulatory T cells in regulating cellular and humoral responses to prevent autoimmunity.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39806065 · DOI · PMC11785521
2'-O-Methyl-guanosine RNA fragments antagonize TLR7 and TLR8 to limit autoimmunity [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Recognition of RNA fragments by Toll-like receptor 7 (TLR7) and TLR8 helps to initiate the innate immune response against pathogens.
- Closing excerpt
- Collectively, this work redefines TLR7 and TLR8 sensing by introducing 2'-OMe guanosine as a natural immune checkpoint for their activation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (146 words)
Recognition of RNA fragments by Toll-like receptor 7 (TLR7) and TLR8 helps to initiate the innate immune response against pathogens. An outstanding question is why RNA fragments generated during clearance of apoptotic cells fail to activate TLR7 and TLR8 signaling. Here we show that select 2'-O-methyl (2'-OMe) guanosine RNA fragments, including those derived from host RNAs, function as potent TLR7 and TLR8 antagonists and reduce TLR7 sensing in vivo. Mechanistically, these fragments bind to an antagonistic site on these proteins via their 5'-end 2'-OMe guanosine. These findings indicate that host RNAs evade detection because abundant ribosomal 2'-OMe-modified fragments naturally antagonize TLR7 and TLR8. Crucially, rare TLR7 and TLR8 mutations at this antagonist binding site decrease inhibition by 2'-OMe guanosine RNA fragments, leading to autoimmunity in patients. Collectively, this work redefines TLR7 and TLR8 sensing by introducing 2'-OMe guanosine as a natural immune checkpoint for their activation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41667621 · DOI · PMC13043311
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Principles of regulatory T cell function [5]
- Research article The intersection of COVID-19 and autoimmunity [6]
- Research article Immune regulatory networks coordinated by glycans and glycan-binding proteins in autoimmunity and infection [7]
- Research article The Impact of Obesity on Thyroid Autoimmunity and Dysfunction: A Systematic Review and Meta-Analysis [8]
- Research article The role of inflammation in autoimmune disease: a therapeutic target [9]
- Research article Zinc Status and Autoimmunity: A Systematic Review and Meta-Analysis [10]
References
- Kong Y, Li J, Zhao X, Wu Y, Chen L. CAR-T cell therapy: developments, challenges and expanded applications from cancer to autoimmunity. . 2024. PMID 39850899 · DOI · PMC11754230
- Nunez SG, Rabelo SP, Subotic N, Caruso JW, Knezevic NN. Chronic Stress and Autoimmunity: The Role of HPA Axis and Cortisol Dysregulation. . 2025. PMID 41155288 · DOI · PMC12563903
- Chen X, Ghanizada M, Mallajosyula V, Sola E, Capasso R, Kathuria KR, et al.. Differential roles of human CD4+ and CD8+ regulatory T cells in controlling self-reactive immune responses. . 2025. PMID 39806065 · DOI · PMC11785521
- Alharbi AS, Sapkota S, Zhang Z, Jin R, Rupasinghe E, Jayasekara WSN, et al.. 2'-O-Methyl-guanosine RNA fragments antagonize TLR7 and TLR8 to limit autoimmunity. . 2026. PMID 41667621 · DOI · PMC13043311
- Dikiy S, Rudensky AY. Principles of regulatory T cell function. Immunity. 2023. PMID 36792571 · DOI
- Knight JS, Caricchio R, Casanova JL, Combes AJ, Diamond B, Fox SE, et al.. The intersection of COVID-19 and autoimmunity. J Clin Invest. 2021. PMID 34710063 · DOI · PMC8670833
- Pinho SS, Alves I, Gaifem J, Rabinovich GA. Immune regulatory networks coordinated by glycans and glycan-binding proteins in autoimmunity and infection. Cell Mol Immunol. 2023. PMID 37582971 · DOI · PMC10541879
- Song RH, Wang B, Yao QM, Li Q, Jia X, Zhang JA. The Impact of Obesity on Thyroid Autoimmunity and Dysfunction: A Systematic Review and Meta-Analysis. Front Immunol. 2019. PMID 31681268 · DOI · PMC6797838
- Xiang Y, Zhang M, Jiang D, Su Q, Shi J. The role of inflammation in autoimmune disease: a therapeutic target. Front Immunol. 2023. PMID 37859999 · DOI · PMC10584158
- Sanna A, Firinu D, Zavattari P, Valera P. Zinc Status and Autoimmunity: A Systematic Review and Meta-Analysis. Nutrients. 2018. PMID 29324654 · DOI · PMC5793296
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.