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Autoimmune Diseases

Immunology · NLM MeSH · updated 2026-10-29 · version 1

Citations verified against PubMedNot yet clinician-reviewed9 referencesApproximately 4 min read

Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

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: 3 complete abstracts (814 words), 9 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

Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.

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: Disease, Autoimmune; Diseases, Autoimmune; Autoimmune Disease.

Where it fits in the MeSH classification

Broader topics
Immune System Diseases
Narrower topics
Addison Disease; Anemia, Hemolytic, Autoimmune; Anti-Glomerular Basement Membrane Disease; Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis; Antiphospholipid Syndrome; Arthritis, Juvenile; Arthritis, Rheumatoid; Autoimmune Diseases of the Nervous System; Autoimmune Hypophysitis; Autoimmune-Inflammatory Syndrome Induced by Adjuvants; Autoimmune Inner Ear Disease; Autoimmune Lymphoproliferative Syndrome; Autoimmune Pancreatitis; Birdshot Chorioretinopathy
See also
Autoantibodies; Autoimmunity

Research landscape

PubMed indexes 604,741 records tagged with the MeSH heading “Autoimmune Diseases” (counts retrieved 2026-10-29). 125,437 of them (20.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 210,431 records.

Reviews account for 101,914 records (16.9%) and meta-analyses for 6,295. Randomized controlled trials number 14,094 (2.3%) as a share of all records on the topic.

PubMed records by publication periodthrough 1999: 210,431 records; 2000-2009: 112,227 records; 2010-2019: 156,646 records; 2020 onward: 125,437 records210,431through 1999112,2272000-2009156,6462010-2019125,4372020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 1999210,431
2000-2009112,227
2010-2019156,646
2020 onward125,437
Share of records by publication typeReviews: 16.9 percent; Meta-analyses: 1.0 percent; Randomized controlled trials: 2.3 percentReviews16.9% (101,914)Meta-analyses1.0% (6,295)Randomized controlled trials2.3% (14,094)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 604,741 PubMed records
TypeRecordsShare
Reviews101,91416.9%
Meta-analyses6,2951.0%
Randomized controlled trials14,0942.3%

Method: PubMed query "Autoimmune Diseases"[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 comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Enrichment and Proteomic Profiling of Stromal-Associated Extracellular Vesicle Subpopulations From Arthritic Synovial Fluid by Size-Exclusion Chromatography Coupled to CD90-Directed Immunocapture
Kurth S, Hanser E, Häner-Massimi S, Giaglis S, Geier F, Burri D, et al.
2026Research article
Design not recorded in structured metadata
1cc by
PMID 42814780 · DOI · PMC13626482
Multiple Sclerosis and Viruses: « Liaisons Dangereuses »
Plavina S, Malakovska D, Kalnina J, Trapina I, Leonova E, Habib M, et al.
2026Review article
Design not recorded in structured metadata
0cc by
PMID 42830637 · DOI · PMC13635778
Efficacy and safety of acute-phase immunotherapy for adult autoimmune encephalitis: a systematic review and network meta-analysis
Deng Y, Cai Y, Yang X, Xu L, Chen Y, Liu N, et al.
2026Systematic review
Design not recorded in structured metadata
0cc by
PMID 42908834 · DOI · PMC13683221

Enrichment and Proteomic Profiling of Stromal-Associated Extracellular Vesicle Subpopulations From Arthritic Synovial Fluid by Size-Exclusion Chromatography Coupled to CD90-Directed Immunocapture [1]

Research article Kurth S, Hanser E, Häner-Massimi S, Giaglis S, Geier F, Burri D, et al. · · 2026 · cited 1 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Extracellular vesicles (EVs) are emerging as key mediators of disease-associated intercellular communication and as promising biomarker sources across many disease conditions, including joint disorders such as rheumatoid arthritis (RA) and osteoarthritis (OA).
Closing excerpt
Together, this fit-for-purpose workflow provides a strategy to resolve EV heterogeneity patient synovial fluid and supports future biomarker-oriented studies of defined subpopulations in arthritic diseases.
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 (273 words)

Extracellular vesicles (EVs) are emerging as key mediators of disease-associated intercellular communication and as promising biomarker sources across many disease conditions, including joint disorders such as rheumatoid arthritis (RA) and osteoarthritis (OA). Molecular profiling of synovial tissue has uncovered disease-driving cellular states, but tissue biopsies are invasive and not routinely available. EVs in synovial fluid may offer a minimally invasive and complementary window into joint pathobiology. However, the molecular complexity of synovial fluid and the heterogeneity of EV populations have hindered the analysis of defined disease-relevant EV subsets. To address this challenge, we developed a refined size-exclusion chromatography-ultrafiltration (SEC-UF) workflow coupled to magnetic bead-based immunocapture for targeted enrichment of cell type-associated EV subpopulations from arthritic synovial fluid. As proof-of-concept, we targeted a stromal-associated EV population using CD90/THY1, a surface marker expressed by discrete synovial fibroblasts subsets implicated in arthritis pathobiology. In vitro validation using synovial fibroblast-derived EVs confirmed surface-accessible CD90 and demonstrated selective immunocapture of defined EV subpopulations. Application to patient-derived synovial fluid showed that SEC-UF pre-enrichment improves the robustness of CD90+ EV recovery from this complex biofluid. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) profiling established broad EV-associated proteome coverage in synovial fluid (SF)-EV preparations and identified multiple proteins reflecting the inflamed arthritic synovial environment. Fraction-resolved proteomics enabled comparison of the CD90-immunocaptured SF-EV subset with the non-captured CD90-/CD90low SF-EV pool. Differential proteomics and surfaceome-informed cell-of-origin analysis supported enrichment of stromal-associated surface markers in the CD90+ fraction, whereas the non-captured SF-EV pool retained broader immune-associated and residual stromal EV inputs. Together, this fit-for-purpose workflow provides a strategy to resolve EV heterogeneity patient synovial fluid and supports future biomarker-oriented studies of defined subpopulations in arthritic diseases.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42814780 · DOI · PMC13626482

Multiple Sclerosis and Viruses: « Liaisons Dangereuses » [2]

Review article Plavina S, Malakovska D, Kalnina J, Trapina I, Leonova E, Habib M, et al. · · 2026

Abstract reading summary — source excerpts
Opening excerpt
Multiple sclerosis (MS) is a complex, multifactorial neurodegenerative disease with an aetiology that is still partially elusive.
Closing excerpt
Characterising these viral interactions presents a new research direction for the identification of novel biomarkers and the development of preventative strategies through the targeted control of viral networks.
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 (255 words)

Multiple sclerosis (MS) is a complex, multifactorial neurodegenerative disease with an aetiology that is still partially elusive. Several risk factors are associated with MS development including genetic predisposition and various environmental stressors; however, recently, viral infections have gained significant attention as a crucial environmental trigger. Despite the well-established link between Epstein-Barr virus (EBV) and MS susceptibility, a single-pathogen model fails to clearly characterise the molecular cascades driving the disease, suggesting that the transition from infection to autoimmune response involves more than one viral agent. In this review we examine the speculation that the interactions among different neurotropic viruses could serve a collective causative role in MS, which is under-researched in the literature at present. We summarise contradictory evidence on the role of different viral agents, including the Herpesviridae family (Human Cytomegalovirus, EBV, Herpes Simplex Viruses HSV-1 and HSV-2, and Varicella Zoster Virus), Paramyxoviridae family (Measles Virus and Rubella Virus), Influenza virus, SARS-CoV-2, and Human Endogenous Retroviruses (HERVs). Through interplay within shared molecular pathways, immune modulation, and activation of latent infections, these viruses may collectively influence the inflammatory and demyelinating processes that characterise MS. This review evaluates the etiological role of viral interplay in MS through the cumulative and interactive effects of these pathogens. The available epidemiological, immunological, and experimental data converge on the concept that viral co-exposures act synergistically to shape MS susceptibility in genetically predisposed individuals. Characterising these viral interactions presents a new research direction for the identification of novel biomarkers and the development of preventative strategies through the targeted control of viral networks.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42830637 · DOI · PMC13635778

Efficacy and safety of acute-phase immunotherapy for adult autoimmune encephalitis: a systematic review and network meta-analysis [3]

Systematic review Deng Y, Cai Y, Yang X, Xu L, Chen Y, Liu N, et al. · · 2026

Abstract reading summary — source excerpts
Opening excerpt
BackgroundAutoimmune encephalitis (AE) is an immune-mediated inflammatory disorder of the central nervous system associated with substantial morbidity.
Closing excerpt
uk/PROSPERO/view/CRD420251085606, identifier CRD420251085606.
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 (286 words)

BackgroundAutoimmune encephalitis (AE) is an immune-mediated inflammatory disorder of the central nervous system associated with substantial morbidity. Acute-phase immunotherapy is crucial for improving outcomes, yet the comparative efficacy and safety of available regimens remain unclear. We therefore performed a Bayesian network meta-analysis to compare acute-phase immunotherapeutic strategies for AE.MethodsPubMed, Embase, Web of Science, and the Cochrane Library were searched from inception to October 2025 for studies evaluating acute-phase immunotherapy in AE. A Bayesian network meta-analysis was conducted. The primary outcome was change in the modified Rankin Scale (mRS) after treatment; adverse events were secondary outcomes. Effects were expressed as mean differences (MD) and risk ratios (RRs) with 95% credible intervals (CrIs). The surface under the cumulative ranking curve (SUCRA) was used to rank interventions.ResultsEleven studies (1,359 patients) were included, evaluating seven strategies: intravenous methylprednisolone (IVMP), intravenous immunoglobulin (IVIG), IVMP+IVIG, IVMP+plasma exchange (PE), IVMP+IVIG+PE, IVMP+immunoadsorption (IA), and IVMP+efgartigimod (EFG). For efficacy, IVMP+EFG ranked highest in mRS improvement among the included regimens (MD = -0.99, 95% CrI -1.30 to -0.68; SUCRA = 95%), followed by IVMP+IA (MD = -0.87; SUCRA = 88%). IVMP+PE ranked lowest (MD = 0.32; SUCRA = 0.2%). For safety, IVIG monotherapy had the lowest adverse-event risk (RR = 0.51, 95% CrI 0.24 to 0.97), whereas IVMP+PE had the highest risk (RR = 3.10, 95% CrI 0.92 to 9.60).ConclusionAcute-phase immunotherapy for AE should be individualized by disease severity and antibody subtype. Consistent directional findings were observed in the anti-NMDAR subgroup and, separately, in the subgroup with baseline mRS ≥3. IVMP+EFG and IVMP+IA ranked favorably for short-term functional improvement, although the evidence was based mainly on observational studies and small sample sizes. IVIG remained a reasonable option given its favorable safety profile.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420251085606, identifier CRD420251085606.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42908834 · DOI · PMC13683221

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 Glucagon-like peptide-1 receptor agonist treatment reduces body weight and improves glycaemic outcomes in patients with concurrent overweight/obesity and type 1 diabetes: A systematic review and meta-analysis [4]
    Purcell AR, Zhen XM, Wong J, Glastras SJ · Diabetes Obes Metab · 2026 · cited 10 times (Europe PMC)
  • Research article Autoimmune thyroid disease and human health: a systematic review of Mendelian randomization studies [5]
    Li P, Wang Q, Yang Y, Ding Z · Front Immunol · 2025 · cited 8 times (Europe PMC)
  • Research article Impact of semaglutide use on glycemic and metabolic profile in adults with type 1 diabetes having overweight or obesity: A systematic review and meta-analysis [6]
    Dutta D, Kamrul-Hasan ABM, Jindal R, Mohindra R, Mohindra R, Nagendra L, et al. · Medicine (Baltimore) · 2025 · cited 8 times (Europe PMC)
  • Research article Obesity as a Risk Factor for Autoimmune Diseases: A Systematic Review and Meta-Analysis [7]
    Spatocco I, Mele G, De Rosa G, Fusco C, Ruggiero K, Pellegrini V, et al. · Obesity (Silver Spring) · 2026 · cited 7 times (Europe PMC)
  • Research article Systematic Review and Meta-Analysis of the Clinical Features Associated With Seronegative Autoimmune Encephalitis [8]
    Di Cosmo L, Mulic-Al Bunni S, Goh Y, Przybysz J, Mgbachi VC, Fox H, et al. · Neurol Neuroimmunol Neuroinflamm · 2026 · cited 6 times (Europe PMC)
  • Research article Association between socioeconomic status and diabetic retinopathy in individuals with type 1 diabetes: a systematic review and meta-analysis [9]
    Sebastian-Valles F, de Arenas-Arroyo SN, Simó-Servat O, Simó R, Painter H, Arranz Martín JA, et al. · BMC Med · 2025 · cited 6 times (Europe PMC)

References

  1. Kurth S, Hanser E, Häner-Massimi S, Giaglis S, Geier F, Burri D, et al.. Enrichment and Proteomic Profiling of Stromal-Associated Extracellular Vesicle Subpopulations From Arthritic Synovial Fluid by Size-Exclusion Chromatography Coupled to CD90-Directed Immunocapture. . 2026. PMID 42814780 · DOI · PMC13626482
  2. Plavina S, Malakovska D, Kalnina J, Trapina I, Leonova E, Habib M, et al.. Multiple Sclerosis and Viruses: « Liaisons Dangereuses ». . 2026. PMID 42830637 · DOI · PMC13635778
  3. Deng Y, Cai Y, Yang X, Xu L, Chen Y, Liu N, et al.. Efficacy and safety of acute-phase immunotherapy for adult autoimmune encephalitis: a systematic review and network meta-analysis. . 2026. PMID 42908834 · DOI · PMC13683221
  4. Purcell AR, Zhen XM, Wong J, Glastras SJ. Glucagon-like peptide-1 receptor agonist treatment reduces body weight and improves glycaemic outcomes in patients with concurrent overweight/obesity and type 1 diabetes: A systematic review and meta-analysis. Diabetes Obes Metab. 2026. PMID 41334580 · DOI · PMC12673429
  5. Li P, Wang Q, Yang Y, Ding Z. Autoimmune thyroid disease and human health: a systematic review of Mendelian randomization studies. Front Immunol. 2025. PMID 41425574 · DOI · PMC12711731
  6. Dutta D, Kamrul-Hasan ABM, Jindal R, Mohindra R, Mohindra R, Nagendra L, et al.. Impact of semaglutide use on glycemic and metabolic profile in adults with type 1 diabetes having overweight or obesity: A systematic review and meta-analysis. Medicine (Baltimore). 2025. PMID 41398803 · DOI · PMC12708229
  7. Spatocco I, Mele G, De Rosa G, Fusco C, Ruggiero K, Pellegrini V, et al.. Obesity as a Risk Factor for Autoimmune Diseases: A Systematic Review and Meta-Analysis. Obesity (Silver Spring). 2026. PMID 41186974 · DOI · PMC12724045
  8. Di Cosmo L, Mulic-Al Bunni S, Goh Y, Przybysz J, Mgbachi VC, Fox H, et al.. Systematic Review and Meta-Analysis of the Clinical Features Associated With Seronegative Autoimmune Encephalitis. Neurol Neuroimmunol Neuroinflamm. 2026. PMID 41499723 · DOI · PMC12794537
  9. Sebastian-Valles F, de Arenas-Arroyo SN, Simó-Servat O, Simó R, Painter H, Arranz Martín JA, et al.. Association between socioeconomic status and diabetic retinopathy in individuals with type 1 diabetes: a systematic review and meta-analysis. BMC Med. 2025. PMID 41350871 · DOI · PMC12798038

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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At a glance

604,741
PubMed records on this heading
21%
published since 2020
101,914
review articles
14,094
randomized trials
9
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

Related topics See all →

  • AutoimmunityImmunology
  • Immunoglobulin G4-Related DiseaseImmunology
  • Graves DiseaseImmunology
  • MyelitisInfectious Diseases
  • Acute Generalized Exanthematous PustulosisImmunology

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