ReviewClinical rheumatology2014
An update on the contribution of the MHC to AS susceptibility.
Review in Clinical rheumatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 59 citations in OpenAlex.
- Autoimmune HLA alleles and neoantigens predict myelodysplastic syndrome outcomes after allogeneic HSCT: A CIBMTR analysis.iScience · 2026Article
- Comprehensive overview of alternative medicine in the treatment of ankylosing spondylitis: Symptoms, pathogenesis, diagnosis and treatments (Review).Biomedical reports · 2026Review
- Review
- MICA and NLRP3 gene polymorphisms interact synergistically affecting the risk of ankylosing spondylitis.Immunologic research · 2024Article
- Exploration of molecular biomarkers in ankylosing spondylitis transcriptomics.Frontiers in immunology · 2024Article
- Investigating potential novel therapeutic targets and biomarkers for ankylosing spondylitis using plasma protein screening.Frontiers in immunology · 2024Article
- Review
- Article
- Role of HLA class I and II alleles in susceptibility to ankylosing spondylitis in Chinese Han.Journal of clinical laboratory analysis · 2023Article
- Screening and identification of key chromatin regulator biomarkers for ankylosing spondylitis and drug prediction: evidence from bioinformatics analysis.BMC musculoskeletal disorders · 2023Article
- How Has Molecular Biology Enhanced Our Undertaking of axSpA and Its Management.Current rheumatology reports · 2023Review
- Genome-wide association study reveals ethnicity-specific SNPs associated with ankylosing spondylitis in the Taiwanese population.Journal of translational medicine · 2022Article
- Outcomes in Juvenile-Onset Spondyloarthritis.Frontiers in medicine · 2021Review
- Association of ProtectiveFrontiers in genetics · 2021Article
- Genetics, Epigenetics, and Gender Impact in Axial-Spondyloarthritis Susceptibility: An Update on Genetic Polymorphisms and Their Sex Related Associations.Frontiers in genetics · 2021Review
- A Mechanism Underlying Sex-Associated Differences in Ankylosing Spondylitis: Troponin C2, Fast Skeletal Type (TNNC2) and Calcium Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- HLA testing in the molecular diagnostic laboratory.Virchows Archiv : an international journal of pathology · 2019Review
- Ankylosing spondylitis: etiology, pathogenesis, and treatments.Bone research · 2019Article
- Human HLA-B27 typing using the BD™ HLA-B27 kit on the BD FACSVia™ system: A multicenter study.Cytometry. Part B, Clinical cytometry · 2018Article
- Identification of ANKDD1B variants in an ankylosing spondylitis pedigree and a sporadic patient.BMC medical genetics · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The 40-year-old association of HLA-B27 with ankylosing spondylitis is one of the best examples of disease association with a hereditary marker. Genomewide association and family studies suggest that other important major histocompatibility complex (MHC) influences are operative in ankylosing spondylitis (AS) susceptibility. HLA-B27 positive hepatitis C individuals are immunologically more efficient in combating viral infections such as HIV-1, hepatitis C, and influenza and less efficient in combating against certain bacteria (and perhaps other organisms) capable of surviving intracellularly. A recent representative population survey of the frequency of HLA-B27 in the USA found a lower frequency of HLA-B27 in older US adults, perhaps reflecting this. Other HLA class I and class II alleles have been implicated in AS susceptibility, the most consistent being HLA-B*40/B60 (B*40:01) but also B14, B15, A*0201, DRB1*04:04, and certain DPA1 and DPB1 alleles. Non-HLA MHC alleles have also been implicated, although many such studies have been inconsistent, likely due to power issues related to the low number of HLA-B27-negative AS patients examined. The best evidence is for major histocompatibility complex class I chain-related gene A (MICA) whose recognition by intestinal epithelial T cells expressing different V-delta-1 gamma/delta TCR further implicates the gut in AS pathogenesis. The HLA class I and class II and other non-HLA allelic associations underscore the importance of T cells in AS pathogenesis.
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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.