Sclerotic-Type Cutaneous Chronic Graft-Versus-Host Disease Exhibits Activation of T Helper 1 and OX40 Cytokines
Sclerotic-type cutaneous chronic graft-versus-host disease is a severe complication of allogeneic hematopoietic stem cell transplantation, with profound morbidity. A dearth of effective, targeted treatment options necessitates further investigation into the molecular mechanisms underlying this T-cel...
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| Veröffentlicht in: | Journal of investigative dermatology 2024-03, Vol.144 (3), p.563-572.e9 |
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| creator | Kim, Madeline Renert-Yuval, Yael Stepensky, Polina Even-Or, Ehud Zaidman, Irina Fachler, Tahel Neumark, Michal Zamir, Mariana NandyMazumdar, Monali Gour, Digpal Facheris, Paola Carroll, Britta Liu, Ying Yu Ekey, Mitchelle L. Andrews, Elizabeth Meariman, Marguerite Angelov, Michael Bose, Swaroop Estrada, Yeriel D. Molho-Pessach, Vered Guttman-Yassky, Emma |
| description | Sclerotic-type cutaneous chronic graft-versus-host disease is a severe complication of allogeneic hematopoietic stem cell transplantation, with profound morbidity. A dearth of effective, targeted treatment options necessitates further investigation into the molecular mechanisms underlying this T-cell–mediated disease. In this study, we compared the transcriptome in skin biopsies from pediatric and young adult (aged 1.5 and false discovery rate < 0.05. Sclerotic-type cutaneous chronic graft-versus-host disease exhibited strong and significant T helper (Th)1 skewing through key related cytokines and chemokines (CXCL9/10/11, IFNG/IFN-γ, STAT1/signal transducer and activator of transcription 1). Several markers related to the TSLP–OX40 axis were significantly upregulated relative to those in both controls and lesional atopic dermatitis, including TNFSF4/OX40L, TSLP, and IL33, as well as fibroinflammatory signatures characterized in a prior study in systemic sclerosis. Gene set variation analysis reflected marker-level findings, showing the greatest enrichment of the Th1 and fibroinflammatory pathways, with no global activation identified in Th2 or Th17/Th22. Cell-type deconvolution revealed a significant representation of macrophages and vascular endothelial cells. Sclerotic-type cutaneous chronic graft-versus-host disease in young patients may therefore be characterized by strong Th1-related upregulation with a unique TSLP–OX40 signature, suggesting new therapeutic avenues for this devastating disease. |
| doi_str_mv | 10.1016/j.jid.2023.08.026 |
| format | Article |
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A dearth of effective, targeted treatment options necessitates further investigation into the molecular mechanisms underlying this T-cell–mediated disease. In this study, we compared the transcriptome in skin biopsies from pediatric and young adult (aged <25 years) patients with sclerotic-type cutaneous chronic graft-versus-host disease (n = 7) with that in demographically matched healthy controls (n = 8) and patients with atopic dermatitis (n = 10) using RNA sequencing with RT-PCR and immunohistochemistry validation. Differential expression was defined as fold change > 1.5 and false discovery rate < 0.05. Sclerotic-type cutaneous chronic graft-versus-host disease exhibited strong and significant T helper (Th)1 skewing through key related cytokines and chemokines (CXCL9/10/11, IFNG/IFN-γ, STAT1/signal transducer and activator of transcription 1). Several markers related to the TSLP–OX40 axis were significantly upregulated relative to those in both controls and lesional atopic dermatitis, including TNFSF4/OX40L, TSLP, and IL33, as well as fibroinflammatory signatures characterized in a prior study in systemic sclerosis. Gene set variation analysis reflected marker-level findings, showing the greatest enrichment of the Th1 and fibroinflammatory pathways, with no global activation identified in Th2 or Th17/Th22. Cell-type deconvolution revealed a significant representation of macrophages and vascular endothelial cells. Sclerotic-type cutaneous chronic graft-versus-host disease in young patients may therefore be characterized by strong Th1-related upregulation with a unique TSLP–OX40 signature, suggesting new therapeutic avenues for this devastating disease.</description><identifier>ISSN: 0022-202X</identifier><identifier>ISSN: 1523-1747</identifier><identifier>EISSN: 1523-1747</identifier><identifier>DOI: 10.1016/j.jid.2023.08.026</identifier><identifier>PMID: 37742913</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Bronchiolitis Obliterans Syndrome ; Child ; Cytokines - metabolism ; Dermatitis, Atopic - genetics ; Dermatitis, Atopic - pathology ; Endothelial Cells - metabolism ; Graft vs Host Disease - genetics ; Humans ; OX40 Ligand ; Skin Diseases ; Th2 Cells - metabolism ; Young Adult</subject><ispartof>Journal of investigative dermatology, 2024-03, Vol.144 (3), p.563-572.e9</ispartof><rights>2023 The Authors</rights><rights>Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c276t-6af8801fc73cda21d8958aa540047942bb33da385553863eb24ad826d8e81ce83</cites><orcidid>0009-0007-9951-4915 ; 0000-0002-8108-3631 ; 0009-0000-2213-2651 ; 0009-0001-3120-0879 ; 0009-0003-0154-283X ; 0000-0001-7272-7143 ; 0000-0002-2371-6058 ; 0000-0001-5346-611X ; 0000-0002-4923-3660 ; 0009-0007-5348-4669 ; 0000-0001-6208-0489 ; 0000-0002-4292-6376 ; 0000-0002-9363-324X ; 0000-0002-8849-5858 ; 0000-0002-5171-9854 ; 0000-0002-5172-6747 ; 0000-0002-3028-0440 ; 0000-0001-5931-3106 ; 0000-0002-4337-9490 ; 0000-0002-2876-3048 ; 0009-0002-6908-2211</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,782,786,887,27931,27932</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37742913$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Madeline</creatorcontrib><creatorcontrib>Renert-Yuval, Yael</creatorcontrib><creatorcontrib>Stepensky, Polina</creatorcontrib><creatorcontrib>Even-Or, Ehud</creatorcontrib><creatorcontrib>Zaidman, Irina</creatorcontrib><creatorcontrib>Fachler, Tahel</creatorcontrib><creatorcontrib>Neumark, Michal</creatorcontrib><creatorcontrib>Zamir, Mariana</creatorcontrib><creatorcontrib>NandyMazumdar, Monali</creatorcontrib><creatorcontrib>Gour, Digpal</creatorcontrib><creatorcontrib>Facheris, Paola</creatorcontrib><creatorcontrib>Carroll, Britta</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Yu Ekey, Mitchelle L.</creatorcontrib><creatorcontrib>Andrews, Elizabeth</creatorcontrib><creatorcontrib>Meariman, Marguerite</creatorcontrib><creatorcontrib>Angelov, Michael</creatorcontrib><creatorcontrib>Bose, Swaroop</creatorcontrib><creatorcontrib>Estrada, Yeriel D.</creatorcontrib><creatorcontrib>Molho-Pessach, Vered</creatorcontrib><creatorcontrib>Guttman-Yassky, Emma</creatorcontrib><title>Sclerotic-Type Cutaneous Chronic Graft-Versus-Host Disease Exhibits Activation of T Helper 1 and OX40 Cytokines</title><title>Journal of investigative dermatology</title><addtitle>J Invest Dermatol</addtitle><description>Sclerotic-type cutaneous chronic graft-versus-host disease is a severe complication of allogeneic hematopoietic stem cell transplantation, with profound morbidity. A dearth of effective, targeted treatment options necessitates further investigation into the molecular mechanisms underlying this T-cell–mediated disease. In this study, we compared the transcriptome in skin biopsies from pediatric and young adult (aged <25 years) patients with sclerotic-type cutaneous chronic graft-versus-host disease (n = 7) with that in demographically matched healthy controls (n = 8) and patients with atopic dermatitis (n = 10) using RNA sequencing with RT-PCR and immunohistochemistry validation. Differential expression was defined as fold change > 1.5 and false discovery rate < 0.05. Sclerotic-type cutaneous chronic graft-versus-host disease exhibited strong and significant T helper (Th)1 skewing through key related cytokines and chemokines (CXCL9/10/11, IFNG/IFN-γ, STAT1/signal transducer and activator of transcription 1). Several markers related to the TSLP–OX40 axis were significantly upregulated relative to those in both controls and lesional atopic dermatitis, including TNFSF4/OX40L, TSLP, and IL33, as well as fibroinflammatory signatures characterized in a prior study in systemic sclerosis. Gene set variation analysis reflected marker-level findings, showing the greatest enrichment of the Th1 and fibroinflammatory pathways, with no global activation identified in Th2 or Th17/Th22. Cell-type deconvolution revealed a significant representation of macrophages and vascular endothelial cells. Sclerotic-type cutaneous chronic graft-versus-host disease in young patients may therefore be characterized by strong Th1-related upregulation with a unique TSLP–OX40 signature, suggesting new therapeutic avenues for this devastating disease.</description><subject>Bronchiolitis Obliterans Syndrome</subject><subject>Child</subject><subject>Cytokines - metabolism</subject><subject>Dermatitis, Atopic - genetics</subject><subject>Dermatitis, Atopic - pathology</subject><subject>Endothelial Cells - metabolism</subject><subject>Graft vs Host Disease - genetics</subject><subject>Humans</subject><subject>OX40 Ligand</subject><subject>Skin Diseases</subject><subject>Th2 Cells - metabolism</subject><subject>Young Adult</subject><issn>0022-202X</issn><issn>1523-1747</issn><issn>1523-1747</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU9vEzEQxS1ERdPAB-CCfOSyW__btSMOqFpKg1SphwbUm-W1Z4nDZh1sb0S-PRulVPTS0xzmvTej90PoPSUlJbS-3JQb70pGGC-JKgmrX6EZrRgvqBTyNZoRwlgxrR_O0UVKGzJ5RKXeoHMupWALymco3NseYsjeFqvDDnAzZjNAGBNu1jEM3uKbaLpc_ICYxlQsQ8r4i09gEuDrP2vf-pzwlc1-b7IPAw4dXuEl9DuImGIzOHz3IAhuDjn88gOkt-isM32Cd49zjr5_vV41y-L27uZbc3VbWCbrXNSmU4rQzkpunWHUqUWljKkEIUIuBGtbzp3hqqoqrmoOLRPGKVY7BYpaUHyOPp9yd2O7BWdhyNH0ehf91sSDDsbr55vBr_XPsNeUCiGPsXP08TEhht8jpKy3Plno-1M_mqla1ZJwRSYpPUltDClF6J7uUKKPpPRGT6T0kZQmSk-kJs-H_x98cvxDMwk-nQQw1bT3EHWyHgYLzkewWbvgX4j_C3copJQ</recordid><startdate>20240301</startdate><enddate>20240301</enddate><creator>Kim, Madeline</creator><creator>Renert-Yuval, Yael</creator><creator>Stepensky, Polina</creator><creator>Even-Or, Ehud</creator><creator>Zaidman, Irina</creator><creator>Fachler, Tahel</creator><creator>Neumark, Michal</creator><creator>Zamir, Mariana</creator><creator>NandyMazumdar, Monali</creator><creator>Gour, Digpal</creator><creator>Facheris, Paola</creator><creator>Carroll, Britta</creator><creator>Liu, Ying</creator><creator>Yu Ekey, Mitchelle L.</creator><creator>Andrews, Elizabeth</creator><creator>Meariman, Marguerite</creator><creator>Angelov, Michael</creator><creator>Bose, Swaroop</creator><creator>Estrada, Yeriel D.</creator><creator>Molho-Pessach, Vered</creator><creator>Guttman-Yassky, Emma</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0009-0007-9951-4915</orcidid><orcidid>https://orcid.org/0000-0002-8108-3631</orcidid><orcidid>https://orcid.org/0009-0000-2213-2651</orcidid><orcidid>https://orcid.org/0009-0001-3120-0879</orcidid><orcidid>https://orcid.org/0009-0003-0154-283X</orcidid><orcidid>https://orcid.org/0000-0001-7272-7143</orcidid><orcidid>https://orcid.org/0000-0002-2371-6058</orcidid><orcidid>https://orcid.org/0000-0001-5346-611X</orcidid><orcidid>https://orcid.org/0000-0002-4923-3660</orcidid><orcidid>https://orcid.org/0009-0007-5348-4669</orcidid><orcidid>https://orcid.org/0000-0001-6208-0489</orcidid><orcidid>https://orcid.org/0000-0002-4292-6376</orcidid><orcidid>https://orcid.org/0000-0002-9363-324X</orcidid><orcidid>https://orcid.org/0000-0002-8849-5858</orcidid><orcidid>https://orcid.org/0000-0002-5171-9854</orcidid><orcidid>https://orcid.org/0000-0002-5172-6747</orcidid><orcidid>https://orcid.org/0000-0002-3028-0440</orcidid><orcidid>https://orcid.org/0000-0001-5931-3106</orcidid><orcidid>https://orcid.org/0000-0002-4337-9490</orcidid><orcidid>https://orcid.org/0000-0002-2876-3048</orcidid><orcidid>https://orcid.org/0009-0002-6908-2211</orcidid></search><sort><creationdate>20240301</creationdate><title>Sclerotic-Type Cutaneous Chronic Graft-Versus-Host Disease Exhibits Activation of T Helper 1 and OX40 Cytokines</title><author>Kim, Madeline ; 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A dearth of effective, targeted treatment options necessitates further investigation into the molecular mechanisms underlying this T-cell–mediated disease. In this study, we compared the transcriptome in skin biopsies from pediatric and young adult (aged <25 years) patients with sclerotic-type cutaneous chronic graft-versus-host disease (n = 7) with that in demographically matched healthy controls (n = 8) and patients with atopic dermatitis (n = 10) using RNA sequencing with RT-PCR and immunohistochemistry validation. Differential expression was defined as fold change > 1.5 and false discovery rate < 0.05. Sclerotic-type cutaneous chronic graft-versus-host disease exhibited strong and significant T helper (Th)1 skewing through key related cytokines and chemokines (CXCL9/10/11, IFNG/IFN-γ, STAT1/signal transducer and activator of transcription 1). Several markers related to the TSLP–OX40 axis were significantly upregulated relative to those in both controls and lesional atopic dermatitis, including TNFSF4/OX40L, TSLP, and IL33, as well as fibroinflammatory signatures characterized in a prior study in systemic sclerosis. Gene set variation analysis reflected marker-level findings, showing the greatest enrichment of the Th1 and fibroinflammatory pathways, with no global activation identified in Th2 or Th17/Th22. Cell-type deconvolution revealed a significant representation of macrophages and vascular endothelial cells. 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| ispartof | Journal of investigative dermatology, 2024-03, Vol.144 (3), p.563-572.e9 |
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| language | eng |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Bronchiolitis Obliterans Syndrome Child Cytokines - metabolism Dermatitis, Atopic - genetics Dermatitis, Atopic - pathology Endothelial Cells - metabolism Graft vs Host Disease - genetics Humans OX40 Ligand Skin Diseases Th2 Cells - metabolism Young Adult |
| title | Sclerotic-Type Cutaneous Chronic Graft-Versus-Host Disease Exhibits Activation of T Helper 1 and OX40 Cytokines |
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