We are analyzing https://link.springer.com/article/10.1007/s00109-005-0721-x.

Title:
Gene expression profiling of Japanese psoriatic skin reveals an increased activity in molecular stress and immune response signals | Journal of Molecular Medicine
Description:
Gene expression profiling was performed on biopsies of affected and unaffected psoriatic skin and normal skin from seven Japanese patients to obtain insights into the pathways that control this disease. HUG95A Affymetrix DNA chips that contained oligonucleotide arrays of approximately 12,000 well-characterized human genes were used in the study. The statistical analysis of the Affymetrix data, based on the ranking of the Student t-test statistic, revealed a complex regulation of molecular stress and immune gene responses. The majority of the 266 induced genes in affected and unaffected psoriatic skin were involved with interferon mediation, immunity, cell adhesion, cytoskeleton restructuring, protein trafficking and degradation, RNA regulation and degradation, signalling transduction, apoptosis and atypical epidermal cellular proliferation and differentiation. The disturbances in the normal protein degradation equilibrium of skin were reflected by the significant increase in the gene expression of various protease inhibitors and proteinases, including the induced components of the ATP/ubiquitin-dependent non-lysosomal proteolytic pathway that is involved with peptide processing and presentation to T cells. Some of the up-regulated genes, such as TGM1, IVL, FABP5, CSTA and SPRR, are well-known psoriatic markers involved in atypical epidermal cellular organization and differentiation. In the comparison between the affected and unaffected psoriatic skin, the transcription factor JUNB was found at the top of the statistical rankings for the up-regulated genes in affected skin, suggesting that it has an important but as yet undefined role in psoriasis. Our gene expression data and analysis suggest that psoriasis is a chronic interferon- and T-cell-mediated immune disease of the skin where the imbalance in epidermal cellular structure, growth and differentiation arises from the molecular antiviral stress signals initiating inappropriate immune responses.
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Keywords {🔍}

article, google, scholar, pubmed, skin, psoriasis, expression, gene, psoriatic, cell, cells, dermatol, molecular, analysis, human, pdf, data, profiling, immune, genes, protein, degradation, role, med, exp, privacy, cookies, content, information, journal, medicine, activity, kulski, interferon, differentiation, access, publish, search, japanese, stress, jerzy, akira, affected, control, responses, induced, rna, epidermal, pathway, lesional,

Topics {✒️}

t-cell-mediated immune disease immune gene responses month download article/chapter gene expression profiling tumour necrosis factor-α student t-test statistic signed-rank call algorithms calcium triggers beta-defensin immune response signals transcription factor activation cell cycle-dependent variations high-density oligonucleotide arrays gene expression data pharmacogenomic expression profiling gene microarray analysis transcription factor junb de jong em defective growth control gene expression interferon-gamma inhibition privacy choices/manage cookies cyclin d1 expression epidermal cellular structure lysosomal proteolytic pathway interferon-α production interferon-α sensitivity lesional psoriatic skin full article pdf unaffected psoriatic skin related subjects contained oligonucleotide arrays siani-rose ma interferon signaling pathway premature cell death human epidermal keratinocytes atp/ubiquitin-dependent nk receptor psoriasis lesional skin 100-element oligonucleotide array hidetoshi inoko expression analysis european economic area functional amphipathic groove select immunodominant epitopes mip-3alpha/ccl20 ligand-generating system unique keratinization process accession number gse2737 molecular medicine aims psoriatic markers involved

Questions {❓}

Aractingi S, Briand N, Le Danff C, Viguier M, Bachelez H, Michel L, Dubertret L, Carosella ED (2001) HLA-G and NK receptor are expressed in psoriatic skin: a possible pathway for regulating infiltrating T cells?

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         headline:Gene expression profiling of Japanese psoriatic skin reveals an increased activity in molecular stress and immune response signals
         description:Gene expression profiling was performed on biopsies of affected and unaffected psoriatic skin and normal skin from seven Japanese patients to obtain insights into the pathways that control this disease. HUG95A Affymetrix DNA chips that contained oligonucleotide arrays of approximately 12,000 well-characterized human genes were used in the study. The statistical analysis of the Affymetrix data, based on the ranking of the Student t-test statistic, revealed a complex regulation of molecular stress and immune gene responses. The majority of the 266 induced genes in affected and unaffected psoriatic skin were involved with interferon mediation, immunity, cell adhesion, cytoskeleton restructuring, protein trafficking and degradation, RNA regulation and degradation, signalling transduction, apoptosis and atypical epidermal cellular proliferation and differentiation. The disturbances in the normal protein degradation equilibrium of skin were reflected by the significant increase in the gene expression of various protease inhibitors and proteinases, including the induced components of the ATP/ubiquitin-dependent non-lysosomal proteolytic pathway that is involved with peptide processing and presentation to T cells. Some of the up-regulated genes, such as TGM1, IVL, FABP5, CSTA and SPRR, are well-known psoriatic markers involved in atypical epidermal cellular organization and differentiation. In the comparison between the affected and unaffected psoriatic skin, the transcription factor JUNB was found at the top of the statistical rankings for the up-regulated genes in affected skin, suggesting that it has an important but as yet undefined role in psoriasis. Our gene expression data and analysis suggest that psoriasis is a chronic interferon- and T-cell-mediated immune disease of the skin where the imbalance in epidermal cellular structure, growth and differentiation arises from the molecular antiviral stress signals initiating inappropriate immune responses.
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      headline:Gene expression profiling of Japanese psoriatic skin reveals an increased activity in molecular stress and immune response signals
      description:Gene expression profiling was performed on biopsies of affected and unaffected psoriatic skin and normal skin from seven Japanese patients to obtain insights into the pathways that control this disease. HUG95A Affymetrix DNA chips that contained oligonucleotide arrays of approximately 12,000 well-characterized human genes were used in the study. The statistical analysis of the Affymetrix data, based on the ranking of the Student t-test statistic, revealed a complex regulation of molecular stress and immune gene responses. The majority of the 266 induced genes in affected and unaffected psoriatic skin were involved with interferon mediation, immunity, cell adhesion, cytoskeleton restructuring, protein trafficking and degradation, RNA regulation and degradation, signalling transduction, apoptosis and atypical epidermal cellular proliferation and differentiation. The disturbances in the normal protein degradation equilibrium of skin were reflected by the significant increase in the gene expression of various protease inhibitors and proteinases, including the induced components of the ATP/ubiquitin-dependent non-lysosomal proteolytic pathway that is involved with peptide processing and presentation to T cells. Some of the up-regulated genes, such as TGM1, IVL, FABP5, CSTA and SPRR, are well-known psoriatic markers involved in atypical epidermal cellular organization and differentiation. In the comparison between the affected and unaffected psoriatic skin, the transcription factor JUNB was found at the top of the statistical rankings for the up-regulated genes in affected skin, suggesting that it has an important but as yet undefined role in psoriasis. Our gene expression data and analysis suggest that psoriasis is a chronic interferon- and T-cell-mediated immune disease of the skin where the imbalance in epidermal cellular structure, growth and differentiation arises from the molecular antiviral stress signals initiating inappropriate immune responses.
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