Evidence map›Paper›PMID 33971035›Full record

ArticleHepatology (Baltimore, Md.)2021

Human Leukocyte Antigen Profile Predicts Severity of Autoimmune Liver Disease in Children of European Ancestry.

Yun Ma, Haibin Su, Muhammed Yuksel, Maria Serena Longhi, Mark J McPhail, Pengyun Wang, Sanjay Bansal, Guan-Wee Wong, Jonathon Graham, Li Yang and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Article
  4. Article
  5. Unmet needs in autoimmune liver diseases.Current opinion in immunology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. NovelFrontiers in immunology · 2023
    Article
  16. Article
  17. Autoimmmune hepatitis.Cellular & molecular immunology · 2022
    Review
  18. Review
  19. Article
  20. HLA, gut microbiome and hepatic autoimmunity.Frontiers in immunology · 2022
    Review
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

19 authors at 7 institutions in 6 countries.

Yun Ma *Institute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Haibin Su *Institute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Muhammed YukselInstitute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Maria Serena LonghiInstitute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Mark J McPhailInstitute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Pengyun WangInstitute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Sanjay BansalPaediatric Liver, GI and Nutrition Centre, King's College Hospital, London, United Kingdom.
Guan-Wee WongInstitute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Jonathon GrahamInstitute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.ORCID 0000-0003-1637-7024
Li YangDepartment of Gastroenterology & Hepatology, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0003-3821-9342
Richard J ThompsonInstitute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Derek G DohertyDiscipline of Immunology, School of Medicine, Trinity College Dublin, Dublin, Ireland.
Nedim HadzicPaediatric Liver, GI and Nutrition Centre, King's College Hospital, London, United Kingdom.
Yoh ZenInstitute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Alberto QuagliaInstitute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Michael A HeneghanInstitute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Marianne Samyn *Paediatric Liver, GI and Nutrition Centre, King's College Hospital, London, United Kingdom.
Diego Vergani *Institute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
Giorgina Mieli-Vergani *Institute of Liver Studies, MowatLabs, Department of Inflammation Biology, School of Immunology & Microbial Sciences, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom.
King's College London · GBKing's College Hospital · GBBeth Israel Deaconess Medical Center · USKoç University · TRRoyal Free London NHS Foundation Trust · GBSichuan University · CNTrinity College Dublin · IE

Funding

Immunomodulatory effects of bilirubin are mediated through aryl hydrocarbon receptor, O2 and purinergic pathwaysR01DK108894 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LONGHI, MARIA SERENA · 2017 to 2021
$2.0M
Alterations of aryl hydrocarbon receptor signaling in autoimmune hepatitisR01DK124408 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LONGHI, MARIA SERENA · 2020 to 2022
$1.2M
Medical Research Council G0902288NIDDK NIH HHS R01 DK108894NIDDK NIH HHS R01 DK124408
6 · The paper itself

Abstract

BACKGROUND AND

aimsGenetic predisposition to autoimmune hepatitis (AIH) in adults is associated with possession of human leukocyte antigen (HLA) class I (A*01, B*08) and class II (DRB1*03, -04, -07, or -13) alleles, depending on geographic region. Juvenile autoimmune liver disease (AILD) comprises AIH-1, AIH-2, and autoimmune sclerosing cholangitis (ASC), which are phenotypically different from their adult counterparts. We aimed to define the relationship between HLA profile and disease course, severity, and outcome in juvenile AILD. APPROACH AND

resultsWe studied 236 children of European ancestry (152 female [64%], median age 11.15 years, range 0.8-17), including 100 with AIH-1, 59 with AIH-2, and 77 with ASC. The follow-up period was from 1977 to June 2019 (median 14.5 years). Class I and II HLA genotyping was performed using PCR/sequence-specific primers. HLA B*08, -DRB1*03, and the A1-B8-DR3 haplotype impart predisposition to all three forms of AILD. Homozygosity for DRB1*03 represented the strongest risk factor (8.8). HLA DRB1*04, which independently confers susceptibility to AIH in adults, was infrequent in AIH-1 and ASC, suggesting protection; and DRB1*15 (DR15) was protective against all forms of AILD. Distinct HLA class II alleles predispose to the different subgroups of juvenile AILD: DRB1*03 to AIH-1, DRB1*13 to ASC, and DRB1*07 to AIH-2. Possession of homozygous DRB1*03 or of DRB1*13 is associated with fibrosis at disease onset, and possession of these two genes in addition to DRB1*07 is associated with a more severe disease in all three subgroups.

conclusionsUnique HLA profiles are seen in each subgroup of juvenile AILD. HLA genotype might be useful in predicting responsiveness to immunosuppressive treatment and course.

Indexed as

AdolescentChildChild, PreschoolCholangitis, SclerosingFemaleGenetic Predisposition to DiseaseHepatitis, AutoimmuneHLA-A1 AntigenHLA AntigensHLA-B8 AntigenHLA-DR3 AntigenHLA-DRB1 ChainsHumansInfantMaleSeverity of Illness IndexHLA-A1 AntigenHLA AntigensHLA-B8 AntigenHLA-DR3 AntigenHLA-DRB1 Chains

Identifiers

PMID33971035
PMCPMC8463472
OpenAlexW3160068266

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.