Post-therapeutic relapse of psoriasis after CD11a blockade is associated with T cells and inflammatory myeloid DCs.

<h4>Unlabelled</h4>To understand the development of new psoriasis lesions, we studied a group of moderate-to-severe psoriasis patients who experienced a relapse after ceasing efalizumab (anti-CD11a, Raptiva, Genentech). There were increased CD3(+) T cells, neutrophils, CD11c(+) and CD83(...

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Autores principales:	Leanne M Johnson-Huang, Cara A Pensabene, Kejal R Shah, Katherine C Pierson, Toyoko Kikuchi, Tim Lentini, Patricia Gilleaudeau, Mary Sullivan-Whalen, Inna Cueto, Artemis Khatcherian, Luke A Hyder, Mayte Suárez-Fariñas, James G Krueger, Michelle A Lowes
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/3578f6aa939e4e8fb1132dc90435b9aa
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spelling	oai:doaj.org-article:3578f6aa939e4e8fb1132dc90435b9aa2021-11-18T07:28:32ZPost-therapeutic relapse of psoriasis after CD11a blockade is associated with T cells and inflammatory myeloid DCs.1932-620310.1371/journal.pone.0030308https://doaj.org/article/3578f6aa939e4e8fb1132dc90435b9aa2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22348003/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Unlabelled</h4>To understand the development of new psoriasis lesions, we studied a group of moderate-to-severe psoriasis patients who experienced a relapse after ceasing efalizumab (anti-CD11a, Raptiva, Genentech). There were increased CD3(+) T cells, neutrophils, CD11c(+) and CD83(+) myeloid dendritic cells (DCs), but no increase in CD1c(+) resident myeloid DCs. In relapsed lesions, there were many CD11c(+)CD1c(-), inflammatory myeloid DCs identified by TNFSF10/TRAIL, TNF, and iNOS. CD11c(+) cells in relapsed lesions co-expressed CD14 and CD16 in situ. Efalizumab induced an improvement in many psoriasis genes, and during relapse, the majority of these genes reversed back to a lesional state. Gene Set Enrichment Analysis (GSEA) of the transcriptome of relapsed tissue showed that many of the gene sets known to be present in psoriasis were also highly enriched in relapse. Hence, on ceasing efalizumab, T cells and myeloid cells rapidly enter the skin to cause classic psoriasis.<h4>Trial registration</h4>Clinicaltrials.gov NCT00115076.Leanne M Johnson-HuangCara A PensabeneKejal R ShahKatherine C PiersonToyoko KikuchiTim LentiniPatricia GilleaudeauMary Sullivan-WhalenInna CuetoArtemis KhatcherianLuke A HyderMayte Suárez-FariñasJames G KruegerMichelle A LowesPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 2, p e30308 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Leanne M Johnson-Huang Cara A Pensabene Kejal R Shah Katherine C Pierson Toyoko Kikuchi Tim Lentini Patricia Gilleaudeau Mary Sullivan-Whalen Inna Cueto Artemis Khatcherian Luke A Hyder Mayte Suárez-Fariñas James G Krueger Michelle A Lowes Post-therapeutic relapse of psoriasis after CD11a blockade is associated with T cells and inflammatory myeloid DCs.
description	<h4>Unlabelled</h4>To understand the development of new psoriasis lesions, we studied a group of moderate-to-severe psoriasis patients who experienced a relapse after ceasing efalizumab (anti-CD11a, Raptiva, Genentech). There were increased CD3(+) T cells, neutrophils, CD11c(+) and CD83(+) myeloid dendritic cells (DCs), but no increase in CD1c(+) resident myeloid DCs. In relapsed lesions, there were many CD11c(+)CD1c(-), inflammatory myeloid DCs identified by TNFSF10/TRAIL, TNF, and iNOS. CD11c(+) cells in relapsed lesions co-expressed CD14 and CD16 in situ. Efalizumab induced an improvement in many psoriasis genes, and during relapse, the majority of these genes reversed back to a lesional state. Gene Set Enrichment Analysis (GSEA) of the transcriptome of relapsed tissue showed that many of the gene sets known to be present in psoriasis were also highly enriched in relapse. Hence, on ceasing efalizumab, T cells and myeloid cells rapidly enter the skin to cause classic psoriasis.<h4>Trial registration</h4>Clinicaltrials.gov NCT00115076.
format	article
author	Leanne M Johnson-Huang Cara A Pensabene Kejal R Shah Katherine C Pierson Toyoko Kikuchi Tim Lentini Patricia Gilleaudeau Mary Sullivan-Whalen Inna Cueto Artemis Khatcherian Luke A Hyder Mayte Suárez-Fariñas James G Krueger Michelle A Lowes
author_facet	Leanne M Johnson-Huang Cara A Pensabene Kejal R Shah Katherine C Pierson Toyoko Kikuchi Tim Lentini Patricia Gilleaudeau Mary Sullivan-Whalen Inna Cueto Artemis Khatcherian Luke A Hyder Mayte Suárez-Fariñas James G Krueger Michelle A Lowes
author_sort	Leanne M Johnson-Huang
title	Post-therapeutic relapse of psoriasis after CD11a blockade is associated with T cells and inflammatory myeloid DCs.
title_short	Post-therapeutic relapse of psoriasis after CD11a blockade is associated with T cells and inflammatory myeloid DCs.
title_full	Post-therapeutic relapse of psoriasis after CD11a blockade is associated with T cells and inflammatory myeloid DCs.
title_fullStr	Post-therapeutic relapse of psoriasis after CD11a blockade is associated with T cells and inflammatory myeloid DCs.
title_full_unstemmed	Post-therapeutic relapse of psoriasis after CD11a blockade is associated with T cells and inflammatory myeloid DCs.
title_sort	post-therapeutic relapse of psoriasis after cd11a blockade is associated with t cells and inflammatory myeloid dcs.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/3578f6aa939e4e8fb1132dc90435b9aa
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Post-therapeutic relapse of psoriasis after CD11a blockade is associated with T cells and inflammatory myeloid DCs.

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