Format

Send to

Choose Destination
See comment in PubMed Commons below
Hum Immunol. 2014 Jan;75(1):98-104. doi: 10.1016/j.humimm.2013.09.012. Epub 2013 Sep 30.

Meta-analysis of differentially expressed genes in primary Sjogren's syndrome by using microarray.

Author information

1
Division of Rheumatology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Republic of Korea.
2
Division of Rheumatology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Republic of Korea. Electronic address: lyhcgh@korea.ac.kr.

Abstract

INTRODUCTION:

The purpose of this study was to identify differentially expressed (DE) genes and biological processes associated with changes in gene expression in primary Sjogren's syndrome (pSS).

METHODS:

We performed a meta-analysis using the INMEX program (integrative meta-analysis of expression data) of publicly available microarray GEO datasets of pSS. We performed Gene Ontology (GO) enrichment analyses and pathway analysis using Kyoto Encyclopedia of Genes and Genomes (KEGG).

RESULTS:

Three GEO datasets including 37 cases and 33 controls were available for the meta-analysis. We identified 179 genes across the studies which were consistently DE in pSS (146 up-regulated and 33 down-regulated). The up-regulated gene with the largest effect size (ES) (ES = -2.4228) was SELL (selectin L), whose product is required for the binding and subsequent rolling of leucocytes on endothelial cells to facilitate their migration into secondary lymphoid organs and inflammation sites. The most significant enrichment was in the immune response GO category (P = 2.52 × 10(-25)). The most significant pathway in our KEGG analysis was Epstein-Barr virus infection (P = 9.91 × 10(-06)).

CONCLUSIONS:

Our meta-analysis demonstrated genes that were consistently DE and biological pathways associated with gene expression changes with pSS.

PMID:
24090683
DOI:
10.1016/j.humimm.2013.09.012
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center