Development of Murine Systemic Lupus Erythematosus in the Absence of BAFF.
Journal
Arthritis & rheumatology (Hoboken, N.J.)
ISSN: 2326-5205
Titre abrégé: Arthritis Rheumatol
Pays: United States
ID NLM: 101623795
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
09
01
2019
accepted:
29
08
2019
pubmed:
8
9
2019
medline:
8
5
2020
entrez:
8
9
2019
Statut:
ppublish
Résumé
To determine whether systemic lupus erythematosus (SLE) can develop in the absence of BAFF in an SLE-prone host. Starting with C57BL/6 mice that express a human BCL2 transgene (Tg) in their B cells (thereby rendering B cell survival largely independent of BAFF-triggered signals), we introgressed this Tg into NZM 2328 mice genetically deficient in BAFF (NZM.Baff In comparison to their non-Tg NZM.Baff The role of BAFF in the development of SLE-like disease may be dispensable as long as B cell survival is preserved via a BAFF-independent pathway. This may help explain the limited and variable clinical success with BAFF antagonists in human SLE. Thus, NZM.Baff
Identifiants
pubmed: 31493335
doi: 10.1002/art.41097
pmc: PMC6994329
mid: NIHMS1049043
doi:
Substances chimiques
B-Cell Activating Factor
0
Tnfsf13b protein, mouse
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
292-302Subventions
Organisme : NIAMS NIH HHS
ID : R01 AR072212
Pays : United States
Organisme : Alliance for Lupus Research
Pays : International
Informations de copyright
© 2019, American College of Rheumatology.
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