ReviewRMD open2024
Lymph nodes as gatekeepers of autoimmune diseases.
Review in RMD open, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Age-associated B-cells across the rheumatoid arthritis continuum: from early immunopathogenesis to comorbidities.Frontiers in aging · 2026Review
- Roles of immune cell metabolism in rheumatoid arthritis.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary lymphoid organs such as lymph nodes (LNs) are the home of peripheral tolerance mechanisms which control autoreactive T cells and prevent immune responses to self-antigen. In systemic autoimmunity, there is a clear failure of these peripheral tolerance mechanisms that leads to chronic inflammation and tissue destruction, highlighting the role for LNs as possible gatekeepers of autoimmunity. In recent years there has been a shift in research focus towards tissue sites in autoimmune diseases ranging from type 1 diabetes to rheumatoid arthritis in an effort to better characterise pathogenesis and guide diagnostic and therapeutic decisions. Although this has yielded great insight, it fails to tackle the initial break in tolerance that initiates disease progression which is most likely originating in peripheral LNs. In the majority of autoimmune diseases a preclinical phase is recognised. This is characterised by the presence of autoantibodies, which is indicative of a break in immune tolerance, and the absence of clinically apparent inflammation or tissue destruction. This review explores how our current knowledge of LNs in the preclinical and established phases of autoimmune diseases provides insight into possibly shared pathological mechanisms that drive disease progression and highlight the gaps in our knowledge that may help uncover new therapeutic avenues for intervention and prevention.
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.