Abrogated AID Function Prolongs Survival and Diminishes Renal Pathology in the BXSB Mouse Model of Systemic Lupus Erythematosus.
Journal
Journal of immunology (Baltimore, Md. : 1950)
ISSN: 1550-6606
Titre abrégé: J Immunol
Pays: United States
ID NLM: 2985117R
Informations de publication
Date de publication:
01 03 2020
01 03 2020
Historique:
received:
06
05
2019
accepted:
22
12
2019
pubmed:
29
1
2020
medline:
9
9
2020
entrez:
29
1
2020
Statut:
ppublish
Résumé
Almost a decade has passed since the approval of belimumab, an mAb directed against B lymphocyte stimulation and the first targeted therapy approved for systemic lupus erythematous (SLE) in over 50 y. Although well tolerated, the efficacy of belimumab remains limited and is not labeled for patients suffering from nephritis, the leading cause of patient mortality. We sought to explore alternative targets of autoreactive B lymphocytes through manipulation of affinity maturation. The BXSB/MpJ mouse, a well-established model of human SLE, develops elevated antinuclear Abs and immune complex-mediated nephritis along with other manifestations of SLE-like disease. To limit interfering with critical background genetics, we used CRISPR-Cas9 to disrupt activation-induced cytidine deaminase (AID;
Identifiants
pubmed: 31988182
pii: jimmunol.1900501
doi: 10.4049/jimmunol.1900501
pmc: PMC7033011
mid: NIHMS1547613
doi:
Substances chimiques
AICDA (activation-induced cytidine deaminase)
EC 3.5.4.-
Cytidine Deaminase
EC 3.5.4.5
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1091-1100Subventions
Organisme : NIDDK NIH HHS
ID : K08 DK101735
Pays : United States
Organisme : NIAMS NIH HHS
ID : R03 AR066787
Pays : United States
Informations de copyright
Copyright © 2020 by The American Association of Immunologists, Inc.
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