Gene expression analysis delineates the potential roles of multiple interferons in systemic lupus erythematosus.
Michelle D CatalinaPrathyusha BachaliNicholas S GeraciAmrie C GrammerPeter E LipskyPublished in: Communications biology (2019)
A role for interferon (IFN) in systemic lupus erythematosus (SLE) pathogenesis is inferred from the prominent IFN gene signature (IGS), but the major IFN species and its relationship to disease activity are unknown. A bioinformatic approach employing individual IFN species gene signatures to interrogate SLE microarray datasets demonstrates a putative role for numerous IFN species, with prominent expression of IFNB1 and IFNW signatures. In contrast with other SLE-affected organs, the IGS is less prominent in lupus nephritis. SLE patients with active and inactive disease have readily detectable IGS and the IGS changes synchronously with a monocyte signature but not disease activity, and is significantly related to monocyte transcripts. Monocyte over-expression of three times as many IGS transcripts as T and B cells and IGS retention in monocytes, but not T and B cells from inactive SLE patients contribute to the lack of correlation between the IGS and SLE disease activity.
Keyphrases
- disease activity
- dendritic cells
- systemic lupus erythematosus
- rheumatoid arthritis
- rheumatoid arthritis patients
- ankylosing spondylitis
- immune response
- gene expression
- juvenile idiopathic arthritis
- genome wide
- poor prognosis
- end stage renal disease
- copy number
- dna methylation
- chronic kidney disease
- ejection fraction
- magnetic resonance
- peripheral blood
- risk assessment
- binding protein
- computed tomography
- magnetic resonance imaging
- long non coding rna
- climate change
- bioinformatics analysis