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Basophils contribute to pristane-induced Lupus-like nephritis model
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 pathogen...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5554199/ https://www.ncbi.nlm.nih.gov/pubmed/28801578 http://dx.doi.org/10.1038/s41598-017-08516-7 |
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author | Dema, Barbara Lamri, Yasmine Pellefigues, Christophe Pacreau, Emeline Saidoune, Fanny Bidault, Caroline Karasuyama, Hajime Sacré, Karim Daugas, Eric Charles, Nicolas |
author_facet | Dema, Barbara Lamri, Yasmine Pellefigues, Christophe Pacreau, Emeline Saidoune, Fanny Bidault, Caroline Karasuyama, Hajime Sacré, Karim Daugas, Eric Charles, Nicolas |
author_sort | Dema, Barbara |
collection | PubMed |
description | 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 | Online Article Text |
id | pubmed-5554199 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-55541992017-08-15 Basophils contribute to pristane-induced Lupus-like nephritis model Dema, Barbara Lamri, Yasmine Pellefigues, Christophe Pacreau, Emeline Saidoune, Fanny Bidault, Caroline Karasuyama, Hajime Sacré, Karim Daugas, Eric Charles, Nicolas Sci Rep Article 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. Nature Publishing Group UK 2017-08-11 /pmc/articles/PMC5554199/ /pubmed/28801578 http://dx.doi.org/10.1038/s41598-017-08516-7 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Dema, Barbara Lamri, Yasmine Pellefigues, Christophe Pacreau, Emeline Saidoune, Fanny Bidault, Caroline Karasuyama, Hajime Sacré, Karim Daugas, Eric Charles, Nicolas Basophils contribute to pristane-induced Lupus-like nephritis model |
title | 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_short | Basophils contribute to pristane-induced Lupus-like nephritis model |
title_sort | basophils contribute to pristane-induced lupus-like nephritis model |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5554199/ https://www.ncbi.nlm.nih.gov/pubmed/28801578 http://dx.doi.org/10.1038/s41598-017-08516-7 |
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