Examination of eQTL Polymorphisms Associated with Increased Risk of Progressive Complicated Sarcoidosis in European and African Descent Subjects.

GWAS SNPs Sarcoidosis expression quantitative trait loci (eQTL) polymorphism

Journal

European journal of respiratory medicine
ISSN: 2633-7452
Titre abrégé: Eur J Respir Med
Pays: England
ID NLM: 9918452988506676

Informations de publication

Date de publication:
Dec 2023
Historique:
medline: 23 2 2024
pubmed: 23 2 2024
entrez: 23 2 2024
Statut: ppublish

Résumé

A limited pool of SNPs are linked to the development and severity of sarcoidosis, a systemic granulomatous inflammatory disease. By integrating genome-wide association studies (GWAS) data and expression quantitative trait loci (eQTL) single nuclear polymorphisms (SNPs), we aimed to identify novel sarcoidosis SNPs potentially influencing the development of complicated sarcoidosis. A GWAS (Affymetrix 6.0) involving 209 African-American (AA) and 193 European-American (EA, 75 and 51 complicated cases respectively) and publicly-available GWAS controls (GAIN) was utilized. Annotation of multi-tissue eQTL SNPs present on the GWAS created a pool of ~46,000 eQTL SNPs examined for association with sarcoidosis risk and severity (Logistic Model, Plink). The most significant EA/AA eQTL SNPs were genotyped in a sarcoidosis validation cohort (n=1034) and cross-validated in two independent GWAS cohorts. No single GWAS SNP achieved significance (p<1x10-8), however, analysis of the eQTL/GWAS SNP pool yielded 621 eQTL SNPs (p<10-4) associated with 730 genes that highlighted innate immunity, MHC Class II, and allograft rejection pathways with multiple SNPs validated in an independent sarcoidosis cohort (105 SNPs analyzed) (NOTCH4, IL27RA, BTNL2, ANXA11, HLA-DRB1). These studies confirm significant association of eQTL/GWAS SNPs in EAs and AAs with sarcoidosis risk and severity (complicated sarcoidosis) involving HLA region and innate immunity. Despite the challenge of deciphering the genetic basis for sarcoidosis risk/severity, these results suggest that integrated eQTL/GWAS approaches may identify novel variants/genes and support the contribution of dysregulated innate immune responses to sarcoidosis severity.

Sections du résumé

Background UNASSIGNED
A limited pool of SNPs are linked to the development and severity of sarcoidosis, a systemic granulomatous inflammatory disease. By integrating genome-wide association studies (GWAS) data and expression quantitative trait loci (eQTL) single nuclear polymorphisms (SNPs), we aimed to identify novel sarcoidosis SNPs potentially influencing the development of complicated sarcoidosis.
Methods UNASSIGNED
A GWAS (Affymetrix 6.0) involving 209 African-American (AA) and 193 European-American (EA, 75 and 51 complicated cases respectively) and publicly-available GWAS controls (GAIN) was utilized. Annotation of multi-tissue eQTL SNPs present on the GWAS created a pool of ~46,000 eQTL SNPs examined for association with sarcoidosis risk and severity (Logistic Model, Plink). The most significant EA/AA eQTL SNPs were genotyped in a sarcoidosis validation cohort (n=1034) and cross-validated in two independent GWAS cohorts.
Results UNASSIGNED
No single GWAS SNP achieved significance (p<1x10-8), however, analysis of the eQTL/GWAS SNP pool yielded 621 eQTL SNPs (p<10-4) associated with 730 genes that highlighted innate immunity, MHC Class II, and allograft rejection pathways with multiple SNPs validated in an independent sarcoidosis cohort (105 SNPs analyzed) (NOTCH4, IL27RA, BTNL2, ANXA11, HLA-DRB1). These studies confirm significant association of eQTL/GWAS SNPs in EAs and AAs with sarcoidosis risk and severity (complicated sarcoidosis) involving HLA region and innate immunity.
Conclusion UNASSIGNED
Despite the challenge of deciphering the genetic basis for sarcoidosis risk/severity, these results suggest that integrated eQTL/GWAS approaches may identify novel variants/genes and support the contribution of dysregulated innate immune responses to sarcoidosis severity.

Identifiants

pubmed: 38390497
pmc: PMC10883688

Types de publication

Journal Article

Langues

eng

Pagination

359-371

Déclaration de conflit d'intérêts

Competing interests Joe GN Garcia MD is CEO and Founder of Aqualung Therapeutics Corporation. David R. Moller MD is Chairman and CTO of Sarcoidosis Diagnostic Testing, LLC. All other authors report no conflict of interest.

Auteurs

Nancy G Casanova (NG)

Department of Molecular Medicine, Univeristy of Florida, Scripps, Jupiter FL, USA.

Sara M Camp (SM)

Center for Inflammation Science and Systems Medicine, University of Florida, Wertheim Scripps Research Institute, Jupiter FL, USA.

Manuel L Gonzalez-Garay (ML)

Division of Health Equities, Department of Population Sciences, City of Hope, Duarte, California, USA.

Ken Batai (K)

Cancer Prevention & Control, Roswell Park Comprehensive Cancer Center, Buffalo, NY, USA.

Lori Garman (L)

Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.

Courtney G Montgomery (CG)

Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.

Nathan Ellis (N)

University of Arizona Cancer Center, Tucson, AZ, USA.

Rick Kittles (R)

Division of Health Equities, Department of Population Sciences, City of Hope, Duarte, California, USA.

Christian Bime (C)

Department of Medicine University of Arizona, Tucson, AZ, USA.

Amy P Hsu (AP)

National Institute of Allergy and Infectious Diseases. National Institutes of Health, USA.

Steven Holland (S)

National Institute of Allergy and Infectious Diseases. National Institutes of Health, USA.

Yves A Lussier (YA)

Department of Biomedical Informatics, University of Utah, Salt Lake City, UT, USA.

Jason Karnes (J)

Department of Pharmacology, University of Arizona, College of Pharmacy, Tucson, AZ, USA.

Nadera Sweiss (N)

Department of Medicine University of Illinois, Chicago, IL, USA.

Lisa A Maier (LA)

Department of Medicine National Jewish Health, University of Colorado, Denver, CO, USA.

Laura Koth (L)

Department of Medicine University of California San Francisco, San Francisco, CA, US, USA.

David R Moller (DR)

Department of Medicine Johns Hopkins University School of Medicine, Baltimore Maryland, USA.

Naftali Kaminski (N)

Department of Medicine Yale University School of Medicine, New Haven, CT, USA.

Joe G N Garcia (JGN)

Center for Inflammation Science and Systems Medicine, University of Florida, Wertheim Scripps Research Institute, Jupiter FL, USA.

Classifications MeSH