Table 1.
Authors/Ref | Samples | Findings | Year |
---|---|---|---|
Oestreicher [15] | 24 psoriatic skin biopsies –lesional and uninvolved | 159 DEGs were generated including S100A7, S100A12, elafin, KRT16, KRT17, MMP12, FARP5 | 2001 |
Nattkemper [34] | 25 patients with atopic dermatitis and 25 patients with psoriasis | 18,000 DEGs common between itchy, lesional atopic, and psoriatic skin identified, outofwhich 2000 genes were unique to both AD and psoriasis including CCL-2/3/17/18, IL-6/8/17A/22/23A, S100A9/A15, TRPV1, PLA2 | 2007 |
Yao [47] | 26 paired nonlesional and lesional (all were plaque-type) skin biopsies from 26 psoriatic patients | Type 1 IFNS were significantly elevated in psoriatic lesions suggesting their active signaling in psoriasis | 2008 |
Ainali [43] | 37 patients affected by chronic plaque psoriasis. | A comprehensive analysis of gene expression in paired lesional and non-lesional psoriatic tissue samples revealed different molecular subgroups associated with Wnt, Notch, TGF-beta, ErbB signaling pathways. |
2012 |
Ewald [54] | Four microarray datasets including 54 LS and 43 NL samples | Differentially expressed in AD several genes involved in lipid metabolism including FA2H, critical in maintaining the permeability barrier of epidermis and ELOVL3, encoding a protein involved in the elongation of long chain fatty acids and essential in prevention of trans-epidermal water loss. | 2015 |
Gudjonsson [41] | 58 psoriatic subjects | Uninvolved psoriatic skin exists in a a “prepsoriatic” gene expression signature and downregulation of PPARA, ESR2 and SREBBF1 suggesting decreased lipid biosynthesis and increased innate immunity in uninvolved psoriatic skin. |
2009 |
Gudjonsson [37] | 58 psoriatic subjects | Identified over 600 new transcripts SERPINB4, PI3, DEFB4 and several S100 family members. Comparison of the psoriatic transcriptome to the transcriptomes of cytokine stimulated cultured keratinocytes revealed little overlap with the lesional psoriatic dysregulated transcriptome. |
2010 |
Swindell [50] | 62 lesional skin samples obtained from patients with stable chronic plaque psoriasis. | Variability in cytokine signature was identified by whole genome transcriptional profiling | 2012 |
Suez Farinas [46] | Skin biopsies from 85 paired lesional and non-lesional samples from a cohort of patients with moderate-to-severe psoriasis vulgaris who were not receiving active psoriasis therapy | Identified 2725 genes as being differentially expressed in psoriasis and link to functional pathways associated with metabolic diseases/diabetes and to cardiovascular risk pathways | 2012 |
Li [31] | 92 psoriatic skin biopsies | RNA-seq analysis identified differentially expressed transcripts enriched for lymphoid and/or myeloid signature transcripts and genes induced by IL-17 in keratinocytes. | 2014 |
Swindell [51] | 163 biopsies from psoriatic lesions | Identified 1233 psoriasis-increased DEGs attributing to keratinocyte activity, infiltration of lesions by T-cells, and macrophages (11%). | 2013 |
Tian [53] | 5 microarray data sets, including 193 LS and NL pairs | Several new genes were identified that are involved in cardiovascular development and lipid metabolism. highlighting the relationship between psoriasis and systemic manifestations such as the metabolic syndrome and cardiovascular disease | 2012 |