Severe thymic atrophy in a mouse model of skin inflammation accounts for impaired TNFR1 signaling.

Transgenic mice expressing the caspase-cleaved form of the tyrosine kinase Lyn (LynΔN) develop a TNFα-dependent skin disease that accurately recapitulates human psoriasis. Participation of lymphocytes in this disease was confirmed by backcrossing LynΔN mice on a Rag-1 deficient background. The prese...

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Autores principales:	Nathalie Belhacéne, Parvati Gamas, Diogo Gonçalvès, Marie Jacquin, Marie Beneteau, Arnaud Jacquel, Pascal Colosetti, Jean-Ehrland Ricci, Abdellilah Wakkach, Patrick Auberger, Sandrine Marchetti
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/fb568eaa08fd49bfa4c9ddadfe6c7f54
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spelling	oai:doaj.org-article:fb568eaa08fd49bfa4c9ddadfe6c7f542021-11-18T08:12:19ZSevere thymic atrophy in a mouse model of skin inflammation accounts for impaired TNFR1 signaling.1932-620310.1371/journal.pone.0047321https://doaj.org/article/fb568eaa08fd49bfa4c9ddadfe6c7f542012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23071785/?tool=EBIhttps://doaj.org/toc/1932-6203Transgenic mice expressing the caspase-cleaved form of the tyrosine kinase Lyn (LynΔN) develop a TNFα-dependent skin disease that accurately recapitulates human psoriasis. Participation of lymphocytes in this disease was confirmed by backcrossing LynΔN mice on a Rag-1 deficient background. The present study was therefore conducted to analyze whether modification of lymphocyte homeostasis does occur and participate in the phenotype of LynΔN mice. We show here that LynΔN mice consistently exhibit thymic atrophy that correlates with both a net decrease in the CD4+/CD8+ Double Positive (DP) and an increase in Single Positive (SP) thymocyte sub-populations, but also display an increase of splenic mature B cell. Interestingly, a normal immune phenotype was rescued in a TNFR1 deficient background. Finally, none of these immune alterations was detected in newborn mice before the onset of inflammation. Therefore, we conclude that chronic inflammation can induce thymic atrophy and perturb spleen homeostasis in LynΔN mice through the increased production of TNFα, LTß and TNFR1 signaling.Nathalie BelhacéneParvati GamasDiogo GonçalvèsMarie JacquinMarie BeneteauArnaud JacquelPascal ColosettiJean-Ehrland RicciAbdellilah WakkachPatrick AubergerSandrine MarchettiPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 10, p e47321 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Nathalie Belhacéne Parvati Gamas Diogo Gonçalvès Marie Jacquin Marie Beneteau Arnaud Jacquel Pascal Colosetti Jean-Ehrland Ricci Abdellilah Wakkach Patrick Auberger Sandrine Marchetti Severe thymic atrophy in a mouse model of skin inflammation accounts for impaired TNFR1 signaling.
description	Transgenic mice expressing the caspase-cleaved form of the tyrosine kinase Lyn (LynΔN) develop a TNFα-dependent skin disease that accurately recapitulates human psoriasis. Participation of lymphocytes in this disease was confirmed by backcrossing LynΔN mice on a Rag-1 deficient background. The present study was therefore conducted to analyze whether modification of lymphocyte homeostasis does occur and participate in the phenotype of LynΔN mice. We show here that LynΔN mice consistently exhibit thymic atrophy that correlates with both a net decrease in the CD4+/CD8+ Double Positive (DP) and an increase in Single Positive (SP) thymocyte sub-populations, but also display an increase of splenic mature B cell. Interestingly, a normal immune phenotype was rescued in a TNFR1 deficient background. Finally, none of these immune alterations was detected in newborn mice before the onset of inflammation. Therefore, we conclude that chronic inflammation can induce thymic atrophy and perturb spleen homeostasis in LynΔN mice through the increased production of TNFα, LTß and TNFR1 signaling.
format	article
author	Nathalie Belhacéne Parvati Gamas Diogo Gonçalvès Marie Jacquin Marie Beneteau Arnaud Jacquel Pascal Colosetti Jean-Ehrland Ricci Abdellilah Wakkach Patrick Auberger Sandrine Marchetti
author_facet	Nathalie Belhacéne Parvati Gamas Diogo Gonçalvès Marie Jacquin Marie Beneteau Arnaud Jacquel Pascal Colosetti Jean-Ehrland Ricci Abdellilah Wakkach Patrick Auberger Sandrine Marchetti
author_sort	Nathalie Belhacéne
title	Severe thymic atrophy in a mouse model of skin inflammation accounts for impaired TNFR1 signaling.
title_short	Severe thymic atrophy in a mouse model of skin inflammation accounts for impaired TNFR1 signaling.
title_full	Severe thymic atrophy in a mouse model of skin inflammation accounts for impaired TNFR1 signaling.
title_fullStr	Severe thymic atrophy in a mouse model of skin inflammation accounts for impaired TNFR1 signaling.
title_full_unstemmed	Severe thymic atrophy in a mouse model of skin inflammation accounts for impaired TNFR1 signaling.
title_sort	severe thymic atrophy in a mouse model of skin inflammation accounts for impaired tnfr1 signaling.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/fb568eaa08fd49bfa4c9ddadfe6c7f54
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Severe thymic atrophy in a mouse model of skin inflammation accounts for impaired TNFR1 signaling.

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