Evidence map›Paper›PMID 40599790›Full record

ReviewFrontiers in immunology2025

Decoding the etiology of immune-mediated inflammatory diseases statistically.

Hesham ElAbd, Aya K H Mahdy

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
  2. The role of DAP12 in immune-related inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Hesham ElAbdInstitute of Clinical Molecular Biology, Kiel University and University Hospital Schleswig-Holstein, Kiel, Germany.
Aya K H MahdyInstitute of Clinical Molecular Biology, Kiel University and University Hospital Schleswig-Holstein, Kiel, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune-mediated inflammatory diseases (IMIDs) are incurable pathologies with an increased prevalence. Whereas different risk factors for IMIDs have been identified, such as microbial dysbiosis, diet, Epstein-Barr virus infection, the exact cause of most of these diseases remains unknown and it is thought to be a combination of environmental exposures and genetic predispositions. Despite their different clinical presentation, most IMIDs are genetically associated with variants at multiple immune-related genes, predominately with different human leukocyte antigen (HLA) alleles suggesting a strong pathological involvement of adaptive immune responses. However, antigens causing these diseases remain, in most cases, unknown. Using statistical analyses of the immune repertoire, several markers of antigenic exposures have been associated with IMIDs. Here, we discuss different approaches to identify disease-associated antigenic exposure markers and formulate a framework to test their causal role in IMIDs. We then discuss the potential contribution of risk HLA alleles to diseases development and lastly, we discuss how either antigens causing IMIDs or their signatures on the immune repertoire can be exploited therapeutically.

Indexed as

Immune System DiseasesInflammationAnimalsBiomarkersGenetic Predisposition to DiseaseHLA AntigensHumansRisk FactorsBiomarkersHLA Antigensetiologyimmune-mediated inflammatory diseasesimmune repertoireimmunogeneticsstatistical analysesT-cell repertoire profilingT-cell therapies

Identifiers

PMID40599790
PMCPMC12209366

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.