Table 1.
Psoriasis transcriptomic analyses.
| Year | References | Samples | Key Message | Methodology and Validation |
|---|---|---|---|---|
| 2001 | Oestreicher et al. [59] | 24 psoriatic skin biopsies (lesional and non-lesional) | This first genome-wide analysis following a pharmacological intervention has shown that treatment can influence the effect on gene expression. Recombinant human IL-11 treatment resulted in increased expression of genes such as GATA3, CRIP1 and TNXA, while cyclosporin A significantly decreased the levels of MMP12, CCNF and HBP17. | Microarray (HuGeneFL, Affymetrix Inc, Santa Clara, CA, USA) |
| 2001 | Bowcock et al. [60] | 15 psoriatic skin biopsies (lesional and non-lesional) | Hierarchical clustering analyses showed a strong difference in gene expression between lesional and non-lesional samples, particularly genes expressed by inflammatory cells. These variances are independent of the HLA-Cw*0602 status of the patients. | Microarray (HG-U95A, Affymetrix Inc, Santa Clara, CA, USA) |
| 2003 | Nomura et al. [61] | Skin biopsies from 7 patients with psoriasis and 6 patients with atopic dermatitis (AD) | Study showing for the first time the distinctive pattern of gene expression that characterizes AD versus psoriatic skin lesion. The 18 genes whose expression is increased in AD skin, including the CC chemokines CCL13, CCL18, and CCL27, as well as the 62 genes whose expression is significantly increased in psoriatic skin compared to AD skin, including CCL4, CCL20, CXCL2, CXCL8, and CXCR2, providing a potential signature for the identification of these skin diseases. | Microarray (HG-U95Av2, Affymetrix Inc, Santa Clara, CA, USA) and qRT-PCR |
| 2003 | Zhou et al. [62] | Psoriatic skin biopsies (lesional and non-lesional) | Identification of two new genes in the IL-1 family genes products that are deregulated in psoriatic lesions, namely IL1HY1 and IL1H1. Ontology analyses have also revealed that epidermal differentiation is the only constantly altered process between lesional/non-lesional skin and normal skin. | Microarray (HG-U95A-E, Affymetrix Inc, Santa Clara, CA, USA) and qRT-PCR |
| 2005 | Kulski et al. [63] | 4 psoriatic skin biopsies (lesional and non-lesional) | Gene expression profiling of Japanese psoriatic skin identified up-regulated genes involved in atypical epidermal cellular organization and differentiation, such as TGM1, IVL, FABP5, CSTA and SPRR. JUNB stands out as the most deregulated gene between lesional and non-lesional samples. | Microarray (HG-U95Av2, Affymetrix Inc, Santa Clara, CA, USA) |
| 2007 | Mee et al. [64] | 6 psoriatic skin biopsies and healthy keratinocytes culture treated with cytokines | A significant correlation between upregulated transcripts in psoriatic skin lesions and the ones from IL-1-induced keratinocytes in vitro suggests a dominant innate immune response in the inflammatory environment of psoriatic lesions rather than an adaptive immune response. | Microarray (HuGeneFL and HG-U133A, Affymetrix Inc, Santa Clara, CA, USA) |
| 2007 | Reischl et al. [65] | 20 psoriatic skin biopsies (lesional and non-lesional) | Increased expression of WTN5A in psoriatic lesions. The involvement of Wtn5a in the pathogenesis of psoriasis remains to be elucidated but increased signaling via Wtn5a could lead to the activation of phospholipase C, and subsequently to the stimulation of the protein kinase C and calcineurin pathways. | Microarray (HG-U133A, Affymetrix Inc, Santa Clara, CA, USA) and qRT-PCR |
| 2008 | Yao et al. [66] | 26 psoriatic skin biopsies (lesional and non-lesional) | Type I IFNs as well as IFNAR1 and IFNAR2 are overexpressed in psoriatic lesional skin. The presence of a signature corresponding to induction by type I IFNs in lesional psoriatic skin suggests active signaling in these lesions. | Microarray (HG-U133 Plus 2.0, Affymetrix Inc, Santa Clara, CA, USA) and qRT-PCR |
| 2009 | Gudjonsson et al. [67] | 58 psoriatic skin biopsies (lesional and non-lesional) |
Non-lesional skin could exist in a “pre-psoriatic” state. The decrease in the activity of three transcription factors, namely PPARA, ESR2 and SREBF1, could be linked to the altered expression of genes involved in lipid metabolism. | Microarray (HG-U133 Plus 2.0, Affymetrix Inc, Santa Clara, CA, USA) and qRT-PCR |
| 2010 | Gudjonsson et al. [68] | 58 psoriatic skin biopsies (lesional and non-lesional) | A large-scale study identifying more than 600 previously unreported transcripts. The comparison of this study with the cytokine-stimulated keratinocytes transcriptomes showed moderate overlap with the psoriatic transcriptome, without however representing more than 5.6% of the complete psoriatic transcriptome. | Microarray (HG-U133 Plus 2.0, Affymetrix Inc, Santa Clara, CA, USA) and qRT-PCR |
| 2011 | Joyce et al. [69] | Psoriatic skin biopsies (lesional and non-lesional) | Identification of a variety of new microRNAs by RNA-sequencing (RNA-seq). Of interest are an uncharacterized keratinocyte-derived miRNA, miR-135b, as well as an epidermal infiltration of the specific hematopoietic miRNA, miR-142-3p, in psoriatic lesions. The functions of these newly identified miRNAs are consistent with the inflammatory and hyperproliferative features of psoriasis. | Illumina (GAIIx, Illumina, San Diego, CA, USA) and qRT-PCR |
| 2012 | Suarez-Farinas et al. [70] | 85 psoriatic skin biopsies (lesional and non-lesional) | A study providing a complex molecular definition of moderate-to-severe psoriasis. Ingenuity pathway analysis identified activated transcription factors, such as NROB2, whose function is the downregulation of target genes. This could also explain the PPARa and RAR activation. | Microarray (HG-U133 Plus 2.0, Affymetrix Inc, Santa Clara, CA, USA) and qRT-PCR |
| 2012 | Jabbari et al. [71] | Psoriatic skin biopsies (lesional and non-lesional) | The comparison of DEGs obtained from this study carried out by RNA-seq with those which used microarray technologies revealed a substantial number of previously unrecognized DEGs in psoriatic skin. The data obtained supported the importance of the synergy of the combined action of IL-17 and TNF-α in the pathogenesis of psoriasis. | RNA-seq (GAIIx, Illumina, San Diego, CA, USA) |
| 2014 | Li et al. [72] | 92 psoriatic skin biopsies | RNA-seq has put forward the involvement of transcripts with low expression levels which could not be identified by microarray studies by revealing gene coexpression networks illuminating processes involving keratinocytes, myeloid cells and T cells. | RNA-seq (GAII, Illumina, San Diego, CA, USA) and microarray (HG-U133 Plus 2.0, Affymetrix Inc, Santa Clara, CA, USA) |
| 2016 | Ahn et al. [73] | 18 psoriatic skin biopsies (pre- and post-treatment with adalimumab) | Treatment with a TNF-α inhibitor, such as adalimumab, promotes normalization of disturbed pathways of psoriasis. The top enriched pathways after biological treatment are the regulation of leukocyte mediated cytotoxicity, regulation of cell killing and leukocyte activation. This study also highlights several roles for long non-coding RNAs. | RNA-seq (HiSeq 2000, Illumina, San Diego, CA, USA) |
| 2016 | Swindell et al. [74] | Psoriatic skin biopsies (performed using reads from prior studies) | The psoriasis specificity index developed revealed that psoriasis specific DEGs are mainly expressed by keratinocytes. Moreover, the activation of the IL-17A pathway appears to be a unique characteristic of psoriasis lesions and an inducer of DEGs. | RNA-seq meta-analysis (GSE41745, GSE54456/GSE63979 and GSE66511) |
| 2017 | Swindell et al. [75] | Psoriatic keratinocyte monolayer culture compared to 4 skin biopsies from the same patients (lesional and non-lesional) | Identification of a decrease in the expression of early and late differentiation markers (KRT1, KRT10, FLG, LOR) as well as of differentiation mediators (CAP14, ACER1) in psoriatic monolayer keratinocytes compared to full-thickness psoriatic biopsies, proposing differentiation as a key dysregulated process. A few genes under-expressed in the psoriatic keratinocytes monolayer have been associated with AP-1 binding sites located in the region of the epidermal differentiation complex, suggesting an intrinsic alteration in psoriatic keratinocytes. | RNA-seq (TruSeq mRNA Sample Prep v2 kit, Illumina, San Diego, CA, USA) |
| 2018 | Ahn et al. [76] | Biopsies from scalp (8), palmoplantar (2) and conventional (8) plaque psoriasis | RNA-seq analysis identifies a core set of DEGs common to the scalp, palmoplantar and conventional psoriasis, including genes involved in the activation and proliferation of keratinocytes, such as S100A7A, SPRR2A/B, SERPINB4, S100A9, KRT6, C10orf99, LCE3D/E and IL36G. The psoriasis subtypes show a differential expression level of the DEGs in this core set and displayed differences in IL-17A, IFNγ, and IL-22 production. | RNA-seq (HiSeq, Illumina, San Diego, CA, USA) and flow cytometry |
| 2018 | Cheng et al. [77] | 9 normal and 3 psoriatic epidermis manually separated from the dermis | Characterization of epidermal cell state according to three anatomical sites (scalp, trunk, and foreskin) as well as the psoriatic epidermis using single-cell RNA-seq revealed a discrete set of specialized keratinocytes that exhibit a distinct composition at different anatomic sites. | Single-cell RNA sequencing (HiSeq 2500, HiSeq 4000 or NovaSeq 6000, Illumina, San Diego, CA, USA) |
| 2018 | Nattkemper et al. [78] | 25 psoriatic skin biopsies | Identification of a gene signature associated with itching is described as “itchscriptome”. These genes are expressed by skin cells, immune cells, and nerves. Their products encode mediators and receptors associated with all aspects of the transmission of itching at the peripheral level. | RNA-seq (NextSeq, Illumina, San Diego, CA, USA) |
| 2018 | Qiao et al. [79] | 13 psoriatic skin biopsies | Results shed light on the effect of deregulation of circRNA expression and its potential biological functions in regulating immunity, inflammation, and proliferation of psoriasis. The aberrant expression of has_circ_0061012, a circRNA with five miRNA binding sites, may be involved in psoriasis and may be a potential biomarker. | Microarray (human ceRNA array V1.0 4x180K, Shanghai Biotechnology Corporation, Shangai, China) and qRT-PCR |
| 2019 | Devos et al. [80] | 9 psoriatic skin biopsies (lesional and non-lesional, dermis and epidermis) | TNAIP3 is decreased in the human epidermis, but not in the dermis, suggesting that down-regulation of A20/TNFAIP3 is likely due to a decrease in its expression by keratinocytes. IMQ-induced psoriatic A20-deficient mice show that skin inflammation caused by loss of A20 in keratinocytes drives systemic inflammation, thus offering a promising therapeutic target. | Microarray (MDS Analytical Technologies, Sunnyvale, CA, USA) |
| 2019 | Pascali et al. [81] | Keratinocytes enriched from 9 psoriatic skin biopsies (lesional and non-lesional) | Gene set enrichment analysis highlighted the dominance of an IL-22/IL-17A signature in psoriatic keratinocytes transcriptome. MetaCore analysis of DEGs revealed significantly enriched sites for multiple transcription factors. Among these, transcription factors still poorly characterized in the context of psoriasis have been identified, namely TRPS1 and HEY2. This study emphasizes the major contribution of keratinocytes in the molecular changes in psoriasis. | Microarray (HTA 2.0, Affymetrix Inc, Santa Clara, CA, USA) and qRT-PCR |
DEG, differentially expressed genes, the bold highlights studies that confirmed their gene profiling data.