Evidence map›Paper›PMID 36197645›Full record

ReviewCurrent rheumatology reports2022

T cell Repertoire Profiling and the Mechanism by which HLA-B27 Causes Ankylosing Spondylitis.

Jose Garrido-Mesa, Matthew A Brown

Open access · hybridAbstract readReview
In one paragraph

Review in Current rheumatology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
10.4field-weighted citation impact, top 1% of its field
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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

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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 at 1 institution in 1 country.

Jose Garrido-MesaDepartment of Medical and Molecular Genetics, Faculty of Life Sciences and Medicine, King's College London, London, England.
Matthew A BrownDepartment of Medical and Molecular Genetics, Faculty of Life Sciences and Medicine, King's College London, London, England. matt.brown@genomicsengland.co.uk.ORCID 0000-0003-0538-8211
King's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewAnkylosing spondylitis (AS) is strongly associated with the HLA-B27 gene. The canonical function of HLA-B27 is to present antigenic peptides to CD8 lymphocytes, leading to adaptive immune responses. The 'arthritogenic peptide' theory as to the mechanism by which HLA-B27 induces ankylosing spondylitis proposes that HLA-B27 presents peptides derived from exogenous sources such as bacteria to CD8 lymphocytes, which subsequently cross-react with antigens at the site of inflammation of the disease, causing inflammation. This review describes findings of studies in AS involving profiling of T cell expansions and discusses future research opportunities based on these findings. RECENT

findingsConsistent with this theory, there is an expanding body of data showing that expansion of a restricted pool of CD8 lymphocytes is found in most AS patients yet only in a small proportion of healthy HLA-B27 carriers. These exciting findings strongly support the theory that AS is driven by presentation of antigenic peptides to the adaptive immune system by HLA-B27. They point to new potential approaches to identify the exogenous and endogenous antigens involved and to potential therapies for the disease.

Indexed as

HLA-B27 AntigenSpondylitis, AnkylosingCD8-Positive T-LymphocytesHumansInflammationPeptidesHLA-B27 AntigenPeptides

Identifiers

PMID36197645
PMCPMC9666335
OpenAlexW4301586442

What OpenQuestion holds

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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 OpenQuestion graph.