Intrapatient comparison of atopic dermatitis skin transcriptome shows differences between tape‐strips and biopsies
Background Our knowledge of etiopathogenesis of atopic dermatitis (AD) is largely derived from skin biopsies, which are associated with pain, scarring and infection. In contrast, tape‐stripping is a minimally invasive, nonscarring technique to collect skin samples. Methods To construct a global AD s...
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| Veröffentlicht in: | Allergy (Copenhagen) 2024-01, Vol.79 (1), p.80-92 |
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| creator | Del Duca, Ester He, Helen Liu, Ying Pagan, Angel D. David, Eden Cheng, Julia Carroll, Britta Renert‐Yuval, Yael Bar, Jonathan Estrada, Yeriel D. Maari, Catherine Proulx, Etienne Saint‐Cyr Krueger, James G. Bissonnette, Robert Guttman‐Yassky, Emma |
| description | Background
Our knowledge of etiopathogenesis of atopic dermatitis (AD) is largely derived from skin biopsies, which are associated with pain, scarring and infection. In contrast, tape‐stripping is a minimally invasive, nonscarring technique to collect skin samples.
Methods
To construct a global AD skin transcriptomic profile comparing tape‐strips to whole‐skin biopsies, we performed RNA‐seq on tape‐strips and biopsies taken from the lesional skin of 20 moderate‐to‐severe AD patients and the skin of 20 controls. Differentially expressed genes (DEGs) were defined by fold‐change (FCH) ≥2.0 and false discovery rate |
| doi_str_mv | 10.1111/all.15845 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2850717122</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2850717122</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3885-a01111c2c2a5d60533647886e1c168f595a29d2bf3733a2bfe6c38ed8cc078a33</originalsourceid><addsrcrecordid>eNp10b1OHDEQB3ArAoULpOAFIks0SbGcvV6vvSVC4UM6iSbUls87qxh27Y3HpxMdj8Az5kkwuQtFpLiZwj__NZ4h5JSzc17O0o7jOZe6kR_IgotOV13XyQOyYJzJqpFCH5FPiA-MMVV37CM5EkoqpRu-IPk25GRnmz2ETF2cZps8xkDjQG2Os3e0hzSV--yR4qMPtPiALvk5xwko_oxbpL0fBkgQHCBdQ94CFGdn-P38grlQpDb0dO3jjB7whBwOdkT4vK_H5P7q-4_Lm2p1d317ebGqnNBaVpa9_c7Vrrayb5kUom2U1i1wx1s9yE7auuvr9SCUELZUaMtD6LVzTGkrxDH5usudU_y1Acxm8uhgHG2AuEFTa8kUV7yuCz37hz7ETQqlO1NGphlrm1YX9W2nXIqICQYzJz_Z9GQ4M2_NmrIK82cVxX7ZJ27WE_Tv8u_sC1juwNaP8PT_JHOxWu0iXwE6jpVO</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2908006468</pqid></control><display><type>article</type><title>Intrapatient comparison of atopic dermatitis skin transcriptome shows differences between tape‐strips and biopsies</title><source>Wiley-Blackwell Journals</source><creator>Del Duca, Ester ; He, Helen ; Liu, Ying ; Pagan, Angel D. ; David, Eden ; Cheng, Julia ; Carroll, Britta ; Renert‐Yuval, Yael ; Bar, Jonathan ; Estrada, Yeriel D. ; Maari, Catherine ; Proulx, Etienne Saint‐Cyr ; Krueger, James G. ; Bissonnette, Robert ; Guttman‐Yassky, Emma</creator><creatorcontrib>Del Duca, Ester ; He, Helen ; Liu, Ying ; Pagan, Angel D. ; David, Eden ; Cheng, Julia ; Carroll, Britta ; Renert‐Yuval, Yael ; Bar, Jonathan ; Estrada, Yeriel D. ; Maari, Catherine ; Proulx, Etienne Saint‐Cyr ; Krueger, James G. ; Bissonnette, Robert ; Guttman‐Yassky, Emma</creatorcontrib><description>Background
Our knowledge of etiopathogenesis of atopic dermatitis (AD) is largely derived from skin biopsies, which are associated with pain, scarring and infection. In contrast, tape‐stripping is a minimally invasive, nonscarring technique to collect skin samples.
Methods
To construct a global AD skin transcriptomic profile comparing tape‐strips to whole‐skin biopsies, we performed RNA‐seq on tape‐strips and biopsies taken from the lesional skin of 20 moderate‐to‐severe AD patients and the skin of 20 controls. Differentially expressed genes (DEGs) were defined by fold‐change (FCH) ≥2.0 and false discovery rate <0.05.
Results
We detected 4104 (2513 Up; 1591 Down) and 1273 (546 Up; 727 Down) DEGs in AD versus controls, in tape‐strips and biopsies, respectively. Although both techniques captured dysregulation of key immune genes, tape‐strips showed higher FCHs for innate immunity (IL‐1B, IL‐8), dendritic cell (ITGAX/CD11C, FCER1A), Th2 (IL‐13, CCL17, TNFRSF4/OX40), and Th17 (CCL20, CXCL1) products, while biopsies showed higher upregulation of Th22 associated genes (IL‐22, S100As) and dermal cytokines (IFN‐γ, CCL26). Itch‐related genes (IL‐31, TRPV3) were preferentially captured by tape‐strips. Epidermal barrier abnormalities were detected in both techniques, with terminal differentiation defects (FLG2, PSORS1C2) better represented by tape‐strips and epidermal hyperplasia changes (KRT16, MKI67) better detected by biopsies.
Conclusions
Tape‐strips and biopsies capture overlapping but distinct features of the AD molecular signature, suggesting their respective utility for monitoring specific AD‐related immune, itch, and barrier abnormalities in clinical trials and longitudinal studies.
This study presents a global RNA‐seq intrapatient profiling of tape‐strips and whole‐skin biopsies in moderate‐to‐severe AD as compared to healthy subjects. Although both techniques captured dysregulation of key immune genes, tape‐strips showed higher FCHs for innate immunity, dendritic cell, Th2, and Th17 products, while biopsies showed higher upregulation of Th22 associated genes and dermal cytokines. Itch‐related genes were preferentially captured by tape‐strips.Abbreviations: AD, atopic dermatitis; AKR1C3, aldo‐keto reductase family 1 member C3; ANXA, annexin; AOC1, amine oxidase copper containing 1; CAMP, cathelicidin antimicrobial peptide; CCL, C‐C motif chemokine ligand; CD, cluster of differentiation; CXCR, C‐X‐C motif chemokine receptor; CTLA4, cytotoxic T‐lymphocyte associated protein; DC, dendritic cell; DEGS2, delta 4‐desaturase, sphingolipid 2; ELOVL3, ELOVL fatty acid elongase 3; FA2H, fatty acid 2‐hydroxylase; FCER1A, Fc epsilon receptor 1A; FCH, fold chanage; FOXP3, forkhead box P3; GAL, galanin; GJPB, gap junction protein beta; GZMA, granzyme A; IL, interleukin; IL4RA, interleukin‐4 receptor alpha chain; IFNG, interferon gamma; ITG, integrin; ITK, IL‐2 inducible T cell kinase; KI67, marker of proliferation Ki‐67; KLK, kallikrein related peptidase; KRT6B, keratin 6B; LCN2, lipocalin 2; MX1, MX dynamin like GTPase 1; OASL, 2’‐5’‐oligoadenylate synthetase like; OSM, oncostatin M; PI3, peptidase inhibitor 3; OX40, TNF receptor superfamily member 4; S100A, S100 calcium binding protein A; TRPM/V, transient receptor potential cation channel subfamily M/V member; XCL2, X‐C motif chemokine ligand 2</description><identifier>ISSN: 0105-4538</identifier><identifier>ISSN: 1398-9995</identifier><identifier>EISSN: 1398-9995</identifier><identifier>DOI: 10.1111/all.15845</identifier><identifier>PMID: 37577841</identifier><language>eng</language><publisher>Denmark: Blackwell Publishing Ltd</publisher><subject>Atopic dermatitis ; biopsies ; Biopsy ; CD11c antigen ; Clinical trials ; Dendritic cells ; Dermatitis ; Eczema ; Helper cells ; Hyperplasia ; immune ; Innate immunity ; Lymphocytes T ; pruritus ; Skin ; Skin diseases ; tape‐strips ; Transcriptomes ; Transcriptomics ; Tumor necrosis factor</subject><ispartof>Allergy (Copenhagen), 2024-01, Vol.79 (1), p.80-92</ispartof><rights>2023 European Academy of Allergy and Clinical Immunology and John Wiley & Sons Ltd.</rights><rights>Copyright © 2024 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3885-a01111c2c2a5d60533647886e1c168f595a29d2bf3733a2bfe6c38ed8cc078a33</citedby><cites>FETCH-LOGICAL-c3885-a01111c2c2a5d60533647886e1c168f595a29d2bf3733a2bfe6c38ed8cc078a33</cites><orcidid>0000-0002-4913-6705 ; 0000-0002-4752-4667 ; 0000-0002-2876-3048 ; 0000-0002-9363-324X ; 0000-0001-6208-0489 ; 0000-0001-7948-8536 ; 0009-0006-7909-9550 ; 0000-0002-3346-3891 ; 0000-0002-9719-0810 ; 0000-0003-4557-6436 ; 0000-0002-5172-6747 ; 0000-0001-7366-9416 ; 0000-0002-3775-1778 ; 0009-0003-0154-283X ; 0000-0001-5927-6587</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fall.15845$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fall.15845$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27922,27923,45572,45573</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37577841$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Del Duca, Ester</creatorcontrib><creatorcontrib>He, Helen</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Pagan, Angel D.</creatorcontrib><creatorcontrib>David, Eden</creatorcontrib><creatorcontrib>Cheng, Julia</creatorcontrib><creatorcontrib>Carroll, Britta</creatorcontrib><creatorcontrib>Renert‐Yuval, Yael</creatorcontrib><creatorcontrib>Bar, Jonathan</creatorcontrib><creatorcontrib>Estrada, Yeriel D.</creatorcontrib><creatorcontrib>Maari, Catherine</creatorcontrib><creatorcontrib>Proulx, Etienne Saint‐Cyr</creatorcontrib><creatorcontrib>Krueger, James G.</creatorcontrib><creatorcontrib>Bissonnette, Robert</creatorcontrib><creatorcontrib>Guttman‐Yassky, Emma</creatorcontrib><title>Intrapatient comparison of atopic dermatitis skin transcriptome shows differences between tape‐strips and biopsies</title><title>Allergy (Copenhagen)</title><addtitle>Allergy</addtitle><description>Background
Our knowledge of etiopathogenesis of atopic dermatitis (AD) is largely derived from skin biopsies, which are associated with pain, scarring and infection. In contrast, tape‐stripping is a minimally invasive, nonscarring technique to collect skin samples.
Methods
To construct a global AD skin transcriptomic profile comparing tape‐strips to whole‐skin biopsies, we performed RNA‐seq on tape‐strips and biopsies taken from the lesional skin of 20 moderate‐to‐severe AD patients and the skin of 20 controls. Differentially expressed genes (DEGs) were defined by fold‐change (FCH) ≥2.0 and false discovery rate <0.05.
Results
We detected 4104 (2513 Up; 1591 Down) and 1273 (546 Up; 727 Down) DEGs in AD versus controls, in tape‐strips and biopsies, respectively. Although both techniques captured dysregulation of key immune genes, tape‐strips showed higher FCHs for innate immunity (IL‐1B, IL‐8), dendritic cell (ITGAX/CD11C, FCER1A), Th2 (IL‐13, CCL17, TNFRSF4/OX40), and Th17 (CCL20, CXCL1) products, while biopsies showed higher upregulation of Th22 associated genes (IL‐22, S100As) and dermal cytokines (IFN‐γ, CCL26). Itch‐related genes (IL‐31, TRPV3) were preferentially captured by tape‐strips. Epidermal barrier abnormalities were detected in both techniques, with terminal differentiation defects (FLG2, PSORS1C2) better represented by tape‐strips and epidermal hyperplasia changes (KRT16, MKI67) better detected by biopsies.
Conclusions
Tape‐strips and biopsies capture overlapping but distinct features of the AD molecular signature, suggesting their respective utility for monitoring specific AD‐related immune, itch, and barrier abnormalities in clinical trials and longitudinal studies.
This study presents a global RNA‐seq intrapatient profiling of tape‐strips and whole‐skin biopsies in moderate‐to‐severe AD as compared to healthy subjects. Although both techniques captured dysregulation of key immune genes, tape‐strips showed higher FCHs for innate immunity, dendritic cell, Th2, and Th17 products, while biopsies showed higher upregulation of Th22 associated genes and dermal cytokines. Itch‐related genes were preferentially captured by tape‐strips.Abbreviations: AD, atopic dermatitis; AKR1C3, aldo‐keto reductase family 1 member C3; ANXA, annexin; AOC1, amine oxidase copper containing 1; CAMP, cathelicidin antimicrobial peptide; CCL, C‐C motif chemokine ligand; CD, cluster of differentiation; CXCR, C‐X‐C motif chemokine receptor; CTLA4, cytotoxic T‐lymphocyte associated protein; DC, dendritic cell; DEGS2, delta 4‐desaturase, sphingolipid 2; ELOVL3, ELOVL fatty acid elongase 3; FA2H, fatty acid 2‐hydroxylase; FCER1A, Fc epsilon receptor 1A; FCH, fold chanage; FOXP3, forkhead box P3; GAL, galanin; GJPB, gap junction protein beta; GZMA, granzyme A; IL, interleukin; IL4RA, interleukin‐4 receptor alpha chain; IFNG, interferon gamma; ITG, integrin; ITK, IL‐2 inducible T cell kinase; KI67, marker of proliferation Ki‐67; KLK, kallikrein related peptidase; KRT6B, keratin 6B; LCN2, lipocalin 2; MX1, MX dynamin like GTPase 1; OASL, 2’‐5’‐oligoadenylate synthetase like; OSM, oncostatin M; PI3, peptidase inhibitor 3; OX40, TNF receptor superfamily member 4; S100A, S100 calcium binding protein A; TRPM/V, transient receptor potential cation channel subfamily M/V member; XCL2, X‐C motif chemokine ligand 2</description><subject>Atopic dermatitis</subject><subject>biopsies</subject><subject>Biopsy</subject><subject>CD11c antigen</subject><subject>Clinical trials</subject><subject>Dendritic cells</subject><subject>Dermatitis</subject><subject>Eczema</subject><subject>Helper cells</subject><subject>Hyperplasia</subject><subject>immune</subject><subject>Innate immunity</subject><subject>Lymphocytes T</subject><subject>pruritus</subject><subject>Skin</subject><subject>Skin diseases</subject><subject>tape‐strips</subject><subject>Transcriptomes</subject><subject>Transcriptomics</subject><subject>Tumor necrosis factor</subject><issn>0105-4538</issn><issn>1398-9995</issn><issn>1398-9995</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp10b1OHDEQB3ArAoULpOAFIks0SbGcvV6vvSVC4UM6iSbUls87qxh27Y3HpxMdj8Az5kkwuQtFpLiZwj__NZ4h5JSzc17O0o7jOZe6kR_IgotOV13XyQOyYJzJqpFCH5FPiA-MMVV37CM5EkoqpRu-IPk25GRnmz2ETF2cZps8xkDjQG2Os3e0hzSV--yR4qMPtPiALvk5xwko_oxbpL0fBkgQHCBdQ94CFGdn-P38grlQpDb0dO3jjB7whBwOdkT4vK_H5P7q-4_Lm2p1d317ebGqnNBaVpa9_c7Vrrayb5kUom2U1i1wx1s9yE7auuvr9SCUELZUaMtD6LVzTGkrxDH5usudU_y1Acxm8uhgHG2AuEFTa8kUV7yuCz37hz7ETQqlO1NGphlrm1YX9W2nXIqICQYzJz_Z9GQ4M2_NmrIK82cVxX7ZJ27WE_Tv8u_sC1juwNaP8PT_JHOxWu0iXwE6jpVO</recordid><startdate>202401</startdate><enddate>202401</enddate><creator>Del Duca, Ester</creator><creator>He, Helen</creator><creator>Liu, Ying</creator><creator>Pagan, Angel D.</creator><creator>David, Eden</creator><creator>Cheng, Julia</creator><creator>Carroll, Britta</creator><creator>Renert‐Yuval, Yael</creator><creator>Bar, Jonathan</creator><creator>Estrada, Yeriel D.</creator><creator>Maari, Catherine</creator><creator>Proulx, Etienne Saint‐Cyr</creator><creator>Krueger, James G.</creator><creator>Bissonnette, Robert</creator><creator>Guttman‐Yassky, Emma</creator><general>Blackwell Publishing Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4913-6705</orcidid><orcidid>https://orcid.org/0000-0002-4752-4667</orcidid><orcidid>https://orcid.org/0000-0002-2876-3048</orcidid><orcidid>https://orcid.org/0000-0002-9363-324X</orcidid><orcidid>https://orcid.org/0000-0001-6208-0489</orcidid><orcidid>https://orcid.org/0000-0001-7948-8536</orcidid><orcidid>https://orcid.org/0009-0006-7909-9550</orcidid><orcidid>https://orcid.org/0000-0002-3346-3891</orcidid><orcidid>https://orcid.org/0000-0002-9719-0810</orcidid><orcidid>https://orcid.org/0000-0003-4557-6436</orcidid><orcidid>https://orcid.org/0000-0002-5172-6747</orcidid><orcidid>https://orcid.org/0000-0001-7366-9416</orcidid><orcidid>https://orcid.org/0000-0002-3775-1778</orcidid><orcidid>https://orcid.org/0009-0003-0154-283X</orcidid><orcidid>https://orcid.org/0000-0001-5927-6587</orcidid></search><sort><creationdate>202401</creationdate><title>Intrapatient comparison of atopic dermatitis skin transcriptome shows differences between tape‐strips and biopsies</title><author>Del Duca, Ester ; He, Helen ; Liu, Ying ; Pagan, Angel D. ; David, Eden ; Cheng, Julia ; Carroll, Britta ; Renert‐Yuval, Yael ; Bar, Jonathan ; Estrada, Yeriel D. ; Maari, Catherine ; Proulx, Etienne Saint‐Cyr ; Krueger, James G. ; Bissonnette, Robert ; Guttman‐Yassky, Emma</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3885-a01111c2c2a5d60533647886e1c168f595a29d2bf3733a2bfe6c38ed8cc078a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Atopic dermatitis</topic><topic>biopsies</topic><topic>Biopsy</topic><topic>CD11c antigen</topic><topic>Clinical trials</topic><topic>Dendritic cells</topic><topic>Dermatitis</topic><topic>Eczema</topic><topic>Helper cells</topic><topic>Hyperplasia</topic><topic>immune</topic><topic>Innate immunity</topic><topic>Lymphocytes T</topic><topic>pruritus</topic><topic>Skin</topic><topic>Skin diseases</topic><topic>tape‐strips</topic><topic>Transcriptomes</topic><topic>Transcriptomics</topic><topic>Tumor necrosis factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Del Duca, Ester</creatorcontrib><creatorcontrib>He, Helen</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Pagan, Angel D.</creatorcontrib><creatorcontrib>David, Eden</creatorcontrib><creatorcontrib>Cheng, Julia</creatorcontrib><creatorcontrib>Carroll, Britta</creatorcontrib><creatorcontrib>Renert‐Yuval, Yael</creatorcontrib><creatorcontrib>Bar, Jonathan</creatorcontrib><creatorcontrib>Estrada, Yeriel D.</creatorcontrib><creatorcontrib>Maari, Catherine</creatorcontrib><creatorcontrib>Proulx, Etienne Saint‐Cyr</creatorcontrib><creatorcontrib>Krueger, James G.</creatorcontrib><creatorcontrib>Bissonnette, Robert</creatorcontrib><creatorcontrib>Guttman‐Yassky, Emma</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Allergy (Copenhagen)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Del Duca, Ester</au><au>He, Helen</au><au>Liu, Ying</au><au>Pagan, Angel D.</au><au>David, Eden</au><au>Cheng, Julia</au><au>Carroll, Britta</au><au>Renert‐Yuval, Yael</au><au>Bar, Jonathan</au><au>Estrada, Yeriel D.</au><au>Maari, Catherine</au><au>Proulx, Etienne Saint‐Cyr</au><au>Krueger, James G.</au><au>Bissonnette, Robert</au><au>Guttman‐Yassky, Emma</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intrapatient comparison of atopic dermatitis skin transcriptome shows differences between tape‐strips and biopsies</atitle><jtitle>Allergy (Copenhagen)</jtitle><addtitle>Allergy</addtitle><date>2024-01</date><risdate>2024</risdate><volume>79</volume><issue>1</issue><spage>80</spage><epage>92</epage><pages>80-92</pages><issn>0105-4538</issn><issn>1398-9995</issn><eissn>1398-9995</eissn><abstract>Background
Our knowledge of etiopathogenesis of atopic dermatitis (AD) is largely derived from skin biopsies, which are associated with pain, scarring and infection. In contrast, tape‐stripping is a minimally invasive, nonscarring technique to collect skin samples.
Methods
To construct a global AD skin transcriptomic profile comparing tape‐strips to whole‐skin biopsies, we performed RNA‐seq on tape‐strips and biopsies taken from the lesional skin of 20 moderate‐to‐severe AD patients and the skin of 20 controls. Differentially expressed genes (DEGs) were defined by fold‐change (FCH) ≥2.0 and false discovery rate <0.05.
Results
We detected 4104 (2513 Up; 1591 Down) and 1273 (546 Up; 727 Down) DEGs in AD versus controls, in tape‐strips and biopsies, respectively. Although both techniques captured dysregulation of key immune genes, tape‐strips showed higher FCHs for innate immunity (IL‐1B, IL‐8), dendritic cell (ITGAX/CD11C, FCER1A), Th2 (IL‐13, CCL17, TNFRSF4/OX40), and Th17 (CCL20, CXCL1) products, while biopsies showed higher upregulation of Th22 associated genes (IL‐22, S100As) and dermal cytokines (IFN‐γ, CCL26). Itch‐related genes (IL‐31, TRPV3) were preferentially captured by tape‐strips. Epidermal barrier abnormalities were detected in both techniques, with terminal differentiation defects (FLG2, PSORS1C2) better represented by tape‐strips and epidermal hyperplasia changes (KRT16, MKI67) better detected by biopsies.
Conclusions
Tape‐strips and biopsies capture overlapping but distinct features of the AD molecular signature, suggesting their respective utility for monitoring specific AD‐related immune, itch, and barrier abnormalities in clinical trials and longitudinal studies.
This study presents a global RNA‐seq intrapatient profiling of tape‐strips and whole‐skin biopsies in moderate‐to‐severe AD as compared to healthy subjects. Although both techniques captured dysregulation of key immune genes, tape‐strips showed higher FCHs for innate immunity, dendritic cell, Th2, and Th17 products, while biopsies showed higher upregulation of Th22 associated genes and dermal cytokines. Itch‐related genes were preferentially captured by tape‐strips.Abbreviations: AD, atopic dermatitis; AKR1C3, aldo‐keto reductase family 1 member C3; ANXA, annexin; AOC1, amine oxidase copper containing 1; CAMP, cathelicidin antimicrobial peptide; CCL, C‐C motif chemokine ligand; CD, cluster of differentiation; CXCR, C‐X‐C motif chemokine receptor; CTLA4, cytotoxic T‐lymphocyte associated protein; DC, dendritic cell; DEGS2, delta 4‐desaturase, sphingolipid 2; ELOVL3, ELOVL fatty acid elongase 3; FA2H, fatty acid 2‐hydroxylase; FCER1A, Fc epsilon receptor 1A; FCH, fold chanage; FOXP3, forkhead box P3; GAL, galanin; GJPB, gap junction protein beta; GZMA, granzyme A; IL, interleukin; IL4RA, interleukin‐4 receptor alpha chain; IFNG, interferon gamma; ITG, integrin; ITK, IL‐2 inducible T cell kinase; KI67, marker of proliferation Ki‐67; KLK, kallikrein related peptidase; KRT6B, keratin 6B; LCN2, lipocalin 2; MX1, MX dynamin like GTPase 1; OASL, 2’‐5’‐oligoadenylate synthetase like; OSM, oncostatin M; PI3, peptidase inhibitor 3; OX40, TNF receptor superfamily member 4; S100A, S100 calcium binding protein A; TRPM/V, transient receptor potential cation channel subfamily M/V member; XCL2, X‐C motif chemokine ligand 2</abstract><cop>Denmark</cop><pub>Blackwell Publishing Ltd</pub><pmid>37577841</pmid><doi>10.1111/all.15845</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-4913-6705</orcidid><orcidid>https://orcid.org/0000-0002-4752-4667</orcidid><orcidid>https://orcid.org/0000-0002-2876-3048</orcidid><orcidid>https://orcid.org/0000-0002-9363-324X</orcidid><orcidid>https://orcid.org/0000-0001-6208-0489</orcidid><orcidid>https://orcid.org/0000-0001-7948-8536</orcidid><orcidid>https://orcid.org/0009-0006-7909-9550</orcidid><orcidid>https://orcid.org/0000-0002-3346-3891</orcidid><orcidid>https://orcid.org/0000-0002-9719-0810</orcidid><orcidid>https://orcid.org/0000-0003-4557-6436</orcidid><orcidid>https://orcid.org/0000-0002-5172-6747</orcidid><orcidid>https://orcid.org/0000-0001-7366-9416</orcidid><orcidid>https://orcid.org/0000-0002-3775-1778</orcidid><orcidid>https://orcid.org/0009-0003-0154-283X</orcidid><orcidid>https://orcid.org/0000-0001-5927-6587</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0105-4538 |
| ispartof | Allergy (Copenhagen), 2024-01, Vol.79 (1), p.80-92 |
| issn | 0105-4538 1398-9995 1398-9995 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2850717122 |
| source | Wiley-Blackwell Journals |
| subjects | Atopic dermatitis biopsies Biopsy CD11c antigen Clinical trials Dendritic cells Dermatitis Eczema Helper cells Hyperplasia immune Innate immunity Lymphocytes T pruritus Skin Skin diseases tape‐strips Transcriptomes Transcriptomics Tumor necrosis factor |
| title | Intrapatient comparison of atopic dermatitis skin transcriptome shows differences between tape‐strips and biopsies |
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