Human Gene Set: GSE6092_CTRL_VS_BORRELIA_BIRGDOFERI_INF_ENDOTHELIAL_CELL_DN

GSEA and MSigDB Need Your Support

We are preparing a grant proposal to NCI's Information Technology for Cancer Research program for the continued funding of GSEA and MSigDB. Click here to learn how you can help. (show)


Standard name GSE6092_CTRL_VS_BORRELIA_BIRGDOFERI_INF_ENDOTHELIAL_CELL_DN
Systematic name M6708
Brief description Genes down-regulated in endothelial cells: untreated versus exposed to E. burgdoferi.
Full description or abstract Borrelia burgdorferi, the agent of Lyme disease, promotes pro-inflammatory changes in endothelium that lead to the recruitment of leukocytes. The host immune response to infection results in increased levels of IFN-gamma in the serum and lesions of Lyme disease patients that correlate with greater severity of disease. Therefore, the effect of IFN-gamma on the gene expression profile of primary human endothelial cells exposed to B. burgdorferi was determined. B. burgdorferi and IFN-gamma synergistically augmented the expression of 34 genes, seven of which encode chemokines. Six of these (CCL7, CCL8, CX3CL1, CXCL9, CXCL10, and CXCL11) attract T lymphocytes, and one (CXCL2) is specific for neutrophils. Synergistic production of the attractants for T cells was confirmed at the protein level. IL-1beta, TNF-alpha, and LPS also cooperated with IFN-gamma to induce synergistic production of CXCL10 by endothelium, indicating that IFN-gamma potentiates inflammation in concert with a variety of mediators. An in vitro model of the blood vessel wall revealed that an increased number of human T lymphocytes traversed endothelium exposed to B. burgdorferi and IFN-gamma, as compared to unstimulated endothelial monolayers. In contrast, addition of IFN-gamma diminished the migration of neutrophils across B. burgdorferi-activated endothelium. IFN-gamma thus alters gene expression by endothelium exposed to B. burgdorferi in a manner that promotes recruitment of T cells and suppresses that of neutrophils. This modulation may facilitate the development of chronic inflammatory lesions in Lyme disease.
Collection C7: Immunologic Signature
      IMMUNESIGDB: ImmuneSigDB
Source publication Pubmed 17202382   Authors: Dame TM,Orenzoff BL,Palmer LE,Furie MB
Exact source GSE6092_3465_200_DN
Related gene sets (show 9 additional gene sets from the source publication)
External links  
Filtered by similarity ?
Organism Homo sapiens
Contributed by Jernej Godec (Dana-Farber Cancer Institute)
Source platform HUMAN_GENE_SYMBOL
Dataset references (show 1 datasets)
Download gene set format: grp | gmt | xml | json | TSV metadata
Compute overlaps ? (show collections to investigate for overlap with this gene set)
Compendia expression profiles ? GTEx compendium
Human tissue compendium (Novartis)
Global Cancer Map (Broad Institute)
NCI-60 cell lines (National Cancer Institute)
Advanced query Further investigate these 149 genes
Gene families ? Categorize these 149 genes by gene family
Show members (show 200 members mapped to 149 genes)
Version history 7.3: Moved to ImmuneSigDB sub-collection.

See MSigDB license terms here. Please note that certain gene sets have special access terms.