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Identification of Hub Genes and Immune Infiltration in Psoriasis by Bioinformatics Method

BACKGROUND: Psoriasis is a chronic, prolonged, and recurrent skin inflammatory disease. However, the pathogenesis of psoriasis is not completely clear, thus we aimed to explore potential molecular basis of it. METHODS: Two datasets were downloaded from the Gene Expression Omnibus database. After ide...

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Autores principales: Su, Wenxing, Wei, Yuqian, Huang, Biao, Ji, Jiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7886814/
https://www.ncbi.nlm.nih.gov/pubmed/33613635
http://dx.doi.org/10.3389/fgene.2021.606065
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author Su, Wenxing
Wei, Yuqian
Huang, Biao
Ji, Jiang
author_facet Su, Wenxing
Wei, Yuqian
Huang, Biao
Ji, Jiang
author_sort Su, Wenxing
collection PubMed
description BACKGROUND: Psoriasis is a chronic, prolonged, and recurrent skin inflammatory disease. However, the pathogenesis of psoriasis is not completely clear, thus we aimed to explore potential molecular basis of it. METHODS: Two datasets were downloaded from the Gene Expression Omnibus database. After identifying the differentially expressed genes of psoriasis skin lesion samples and healthy controls, three kinds of analyses, namely functional annotation, protein-protein interaction (PPI) network, and immune infiltration analyses, were performed. RESULTS: A total of 152 up-regulated genes and 38 down-regulated genes were selected for subsequent analyses. Evaluation of the PPI network identified the most important module containing 13 hub genes. Gene ontology analysis showed that the hub genes have a significant enrichment effect on positive regulation of cell migration, defense response to the other organism and epithelial cell differentiation. KEGG signaling pathway analysis showed that the hub genes were significantly enriched in chemokine signaling, Toll-like receptor signaling pathway, and IL-17 signaling pathway. Compared with the normal control sample, naive B cells, CD8(+) T cells, activated memory CD4(+) T cells, follicular helper T cells, gamma delta T cells, resting NK cells, monocytes, M0 macrophages, M1 macrophages, activated dendritic cells and neutrophils infiltrated more, while memory B cells, naive CD4(+) T cells, regulatory T cells (Tregs), activated NK cells, resting mast cells, and eosinophils infiltrated less. CONCLUSION: To conclude, the hub genes and pathways identified from psoriasis lesions and normal controls along with the immune infiltration profile may provide new insights into the study of psoriasis.
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spelling pubmed-78868142021-02-18 Identification of Hub Genes and Immune Infiltration in Psoriasis by Bioinformatics Method Su, Wenxing Wei, Yuqian Huang, Biao Ji, Jiang Front Genet Genetics BACKGROUND: Psoriasis is a chronic, prolonged, and recurrent skin inflammatory disease. However, the pathogenesis of psoriasis is not completely clear, thus we aimed to explore potential molecular basis of it. METHODS: Two datasets were downloaded from the Gene Expression Omnibus database. After identifying the differentially expressed genes of psoriasis skin lesion samples and healthy controls, three kinds of analyses, namely functional annotation, protein-protein interaction (PPI) network, and immune infiltration analyses, were performed. RESULTS: A total of 152 up-regulated genes and 38 down-regulated genes were selected for subsequent analyses. Evaluation of the PPI network identified the most important module containing 13 hub genes. Gene ontology analysis showed that the hub genes have a significant enrichment effect on positive regulation of cell migration, defense response to the other organism and epithelial cell differentiation. KEGG signaling pathway analysis showed that the hub genes were significantly enriched in chemokine signaling, Toll-like receptor signaling pathway, and IL-17 signaling pathway. Compared with the normal control sample, naive B cells, CD8(+) T cells, activated memory CD4(+) T cells, follicular helper T cells, gamma delta T cells, resting NK cells, monocytes, M0 macrophages, M1 macrophages, activated dendritic cells and neutrophils infiltrated more, while memory B cells, naive CD4(+) T cells, regulatory T cells (Tregs), activated NK cells, resting mast cells, and eosinophils infiltrated less. CONCLUSION: To conclude, the hub genes and pathways identified from psoriasis lesions and normal controls along with the immune infiltration profile may provide new insights into the study of psoriasis. Frontiers Media S.A. 2021-02-03 /pmc/articles/PMC7886814/ /pubmed/33613635 http://dx.doi.org/10.3389/fgene.2021.606065 Text en Copyright © 2021 Su, Wei, Huang and Ji. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Genetics
Su, Wenxing
Wei, Yuqian
Huang, Biao
Ji, Jiang
Identification of Hub Genes and Immune Infiltration in Psoriasis by Bioinformatics Method
title Identification of Hub Genes and Immune Infiltration in Psoriasis by Bioinformatics Method
title_full Identification of Hub Genes and Immune Infiltration in Psoriasis by Bioinformatics Method
title_fullStr Identification of Hub Genes and Immune Infiltration in Psoriasis by Bioinformatics Method
title_full_unstemmed Identification of Hub Genes and Immune Infiltration in Psoriasis by Bioinformatics Method
title_short Identification of Hub Genes and Immune Infiltration in Psoriasis by Bioinformatics Method
title_sort identification of hub genes and immune infiltration in psoriasis by bioinformatics method
topic Genetics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7886814/
https://www.ncbi.nlm.nih.gov/pubmed/33613635
http://dx.doi.org/10.3389/fgene.2021.606065
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