Basophils contribute to pristane-induced Lupus-like nephritis model - Inserm - Institut national de la santé et de la recherche médicale Accéder directement au contenu
Article Dans Une Revue Scientific Reports Année : 2017

Basophils contribute to pristane-induced Lupus-like nephritis model

Résumé

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.

Domaines

Immunologie
Fichier principal
Vignette du fichier
Dema Lamri Sci Rep 2017.pdf (3.08 Mo) Télécharger le fichier
Origine : Publication financée par une institution
Loading...

Dates et versions

inserm-01590414 , version 1 (19-09-2017)

Identifiants

Citer

Barbara Dema, Yasmine Lamri, Christophe Pellefigues, Emeline Pacreau, Fanny Saidoune, et al.. Basophils contribute to pristane-induced Lupus-like nephritis model. Scientific Reports, 2017, 7 (1), pp.7969. ⟨10.1038/s41598-017-08516-7⟩. ⟨inserm-01590414⟩
191 Consultations
192 Téléchargements

Altmetric

Partager

Gmail Facebook X LinkedIn More