Evidence map›Paper›PMID 35759748›Full record

ArticleJournal of pediatric gastroenterology and nutrition2022

Expression of HLA and Autoimmune Pathway Genes in Liver Biopsies of Young Subjects With Autoimmune Hepatitis Type 1.

Emilia Shin, Kathleen B Schwarz, Lorraine V Jones-Brando, Liliana D Florea, Sarven Sabunciyan, Laura Delong Wood, Robert H Yolken

Open access · hybridAbstract read
In one paragraph

Article in Journal of pediatric gastroenterology and nutrition, 2022. 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
0.7field-weighted citation impact, top 32% 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

6 citing papers in PubMed, 6 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

7 authors at 2 institutions in 1 country.

Emilia ShinFrom the Pediatrics, Johns Hopkins Medical Institutions, Baltimore, MD.
Kathleen B SchwarzFrom the Pediatrics, Johns Hopkins Medical Institutions, Baltimore, MD.
Lorraine V Jones-BrandoFrom the Pediatrics, Johns Hopkins Medical Institutions, Baltimore, MD.
Liliana D Floreathe Genetic Medicine, Johns Hopkins Medical Institutions, Baltimore, MD.
Sarven SabunciyanFrom the Pediatrics, Johns Hopkins Medical Institutions, Baltimore, MD.
Laura Delong Woodthe Pathology, Johns Hopkins Medical Institutions, Baltimore, MD.
Robert H YolkenFrom the Pediatrics, Johns Hopkins Medical Institutions, Baltimore, MD.
Johns Hopkins University · USJohns Hopkins Bayview Medical Center · US

Funding

Computational Methods to Characterize Alternative Splicing from Massive Collections of RNA-seq DataR01GM129085 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI FLOREA, LILIANA D · 2019 to 2022
$1.5M
NIGMS NIH HHS R01 GM129085
6 · The paper itself

Abstract

objectivesTo test the hypothesis that autoimmune hepatitis (AIH type I) in young subjects is due to genetic differences in proinflammatory genes responding to viral triggers in patients and controls.

methodsIntrahepatic gene expression was compared between AIH type I (n = 24, age 9-30 years) patients (hereafter referred to as the AIH group) and controls (n = 21, age 4-25 years). RNA sequencing was performed on complementary DNA (cDNA) libraries made from total RNA extracted from formalin-fixed paraffin-embedded (FFPE) liver biopsy samples. Gene expression levels were quantified, and differentially expressed genes were functionally analyzed. Pathway analysis was performed using the databases Kyoto Encyclopedia of Genes and Genomes (KEGG) and PANTHER. The remaining sequences were mapped to the RefSeq complete set of viral genomes.

resultsDifferential gene analysis identified 181 genes that were significantly differentially expressed (136 upregulated in the AIH group). Autoimmune pathway genes such as CD19 and CD20 which are important in B cell regulation and maturation as well as, CD8 and LY9 , which are T-cell related, were upregulated in our AIH group. Genes implicated in AIH pathogenesis including CXCL10 , which is thought to be associated with AIH severity and progression, complement genes ( C1QA, C1QB , and C1QC ), and human leucocyte antigen ( HLA ) genes ( HLA-DRB1, HLA-DRA, HLA-B , and HLA-C ) were upregulated in samples from the AIH group. Specific viral etiologies were not found.

conclusionsUnbiased next-generation sequencing and differential gene expression analysis of the AIH group has not only added support for the role of B cells in the pathogenesis and treatment of AIH but also has introduced potential new therapeutic targets: CXCL10 (anti- CXCL10 ) and several complement system-related genes.

Indexed as

Hepatitis, AutoimmuneAdolescentAdultBiopsyChildChild, PreschoolGenetic Predisposition to DiseaseHLA-DRB1 ChainsHumansYoung AdultHLA-DRB1 Chains

Identifiers

PMID35759748
PMCPMC9365252
OpenAlexW4283699402

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.