Basophils contribute to pristane-induced Lupus-like nephritis model

Abstract Lupus nephritis (LN), one of the most severe outcomes of systemic lupus erythematosus (SLE), is initiated by glomerular deposition of immune-complexes leading to an inflammatory response and kidney failure. Autoantibodies to nuclear antigens and autoreactive B and T cells are central in SLE...

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Autores principales:	Barbara Dema, Yasmine Lamri, Christophe Pellefigues, Emeline Pacreau, Fanny Saidoune, Caroline Bidault, Hajime Karasuyama, Karim Sacré, Eric Daugas, Nicolas Charles
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/d1e831bfa8914cf4b9b64614988ae423
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spelling	oai:doaj.org-article:d1e831bfa8914cf4b9b64614988ae4232021-12-02T12:32:32ZBasophils contribute to pristane-induced Lupus-like nephritis model10.1038/s41598-017-08516-72045-2322https://doaj.org/article/d1e831bfa8914cf4b9b64614988ae4232017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-08516-7https://doaj.org/toc/2045-2322Abstract Lupus nephritis (LN), one of the most severe outcomes of systemic lupus erythematosus (SLE), is initiated by glomerular deposition of immune-complexes leading to an inflammatory response and kidney failure. Autoantibodies to nuclear antigens and autoreactive B and T cells are central in SLE pathogenesis. Immune mechanisms amplifying this autoantibody production drive flares of the disease. We previously showed that basophils were contributing to LN development in a spontaneous lupus-like mouse model (constitutive Lyn −/− mice) and in SLE subjects through their activation and migration to secondary lymphoid organs (SLOs) where they amplify autoantibody production. In order to study the basophil-specific mechanisms by which these cells contribute to LN development, we needed to validate their involvement in a genetically independent SLE-like mouse model. Pristane, when injected to non-lupus-prone mouse strains, induces a LN-like disease. In this inducible model, basophils were activated and accumulated in SLOs to promote autoantibody production. Basophil depletion by two distinct approaches dampened LN-like disease, demonstrating their contribution to the pristane-induced LN model. These results enable further studies to decipher molecular mechanisms by which basophils contribute to lupus progression.Barbara DemaYasmine LamriChristophe PellefiguesEmeline PacreauFanny SaidouneCaroline BidaultHajime KarasuyamaKarim SacréEric DaugasNicolas CharlesNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-9 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Barbara Dema Yasmine Lamri Christophe Pellefigues Emeline Pacreau Fanny Saidoune Caroline Bidault Hajime Karasuyama Karim Sacré Eric Daugas Nicolas Charles Basophils contribute to pristane-induced Lupus-like nephritis model
description	Abstract Lupus nephritis (LN), one of the most severe outcomes of systemic lupus erythematosus (SLE), is initiated by glomerular deposition of immune-complexes leading to an inflammatory response and kidney failure. Autoantibodies to nuclear antigens and autoreactive B and T cells are central in SLE pathogenesis. Immune mechanisms amplifying this autoantibody production drive flares of the disease. We previously showed that basophils were contributing to LN development in a spontaneous lupus-like mouse model (constitutive Lyn −/− mice) and in SLE subjects through their activation and migration to secondary lymphoid organs (SLOs) where they amplify autoantibody production. In order to study the basophil-specific mechanisms by which these cells contribute to LN development, we needed to validate their involvement in a genetically independent SLE-like mouse model. Pristane, when injected to non-lupus-prone mouse strains, induces a LN-like disease. In this inducible model, basophils were activated and accumulated in SLOs to promote autoantibody production. Basophil depletion by two distinct approaches dampened LN-like disease, demonstrating their contribution to the pristane-induced LN model. These results enable further studies to decipher molecular mechanisms by which basophils contribute to lupus progression.
format	article
author	Barbara Dema Yasmine Lamri Christophe Pellefigues Emeline Pacreau Fanny Saidoune Caroline Bidault Hajime Karasuyama Karim Sacré Eric Daugas Nicolas Charles
author_facet	Barbara Dema Yasmine Lamri Christophe Pellefigues Emeline Pacreau Fanny Saidoune Caroline Bidault Hajime Karasuyama Karim Sacré Eric Daugas Nicolas Charles
author_sort	Barbara Dema
title	Basophils contribute to pristane-induced Lupus-like nephritis model
title_short	Basophils contribute to pristane-induced Lupus-like nephritis model
title_full	Basophils contribute to pristane-induced Lupus-like nephritis model
title_fullStr	Basophils contribute to pristane-induced Lupus-like nephritis model
title_full_unstemmed	Basophils contribute to pristane-induced Lupus-like nephritis model
title_sort	basophils contribute to pristane-induced lupus-like nephritis model
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/d1e831bfa8914cf4b9b64614988ae423
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Basophils contribute to pristane-induced Lupus-like nephritis model

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