期刊
SCIENTIFIC REPORTS
卷 7, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-017-08516-7
关键词
-
资金
- French Institut National de la Sante Et de la Recherche Medicale (INSERM)
- Assistance Publique - Hopitaux de Paris (AP-HP)
- laboratoire d'excellence INFLAMEX
- Departement Hospitalo-Universitaire (DHU) FIRE
- Centre National de la Recherche Scientifique (CNRS)
- Mairie de Paris (Emergences)
- French Kidney Foundation (Fondation du Rein)
- Agence Nationale de la Recherche (ANR) JCJC SVSE1 BASILE
- JCJC CE17 BATTLE
- Grants-in-Aid for Scientific Research [15H05786] Funding Source: KAKEN
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据