SH3BP2 Deficiency Ameliorates Murine Systemic Lupus Erythematosus.
Src homology 3 domain-binding protein 2
dendritic cells
lupus mouse model
systemic lupus erythematosus
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
17 Apr 2021
17 Apr 2021
Historique:
received:
21
02
2021
revised:
15
04
2021
accepted:
16
04
2021
entrez:
30
4
2021
pubmed:
1
5
2021
medline:
13
5
2021
Statut:
epublish
Résumé
The adaptor protein Src homology 3 domain-binding protein 2 (SH3BP2) is widely expressed in immune cells. It controls intracellular signaling pathways. The present study was undertaken to investigate the role of SH3BP2 in a murine systemic lupus erythematosus model. For the lupus model, we used SH3BP2 deficiency significantly reduced lupus-like phenotypes, presented as splenomegaly, renal involvement, elevated serum anti-dsDNA antibody, and increased splenic B220 SH3BP2 deficiency ameliorated lupus-like manifestations. Modulating SH3BP2 expression could thus provide a novel therapeutic approach to autoimmune diseases.
Sections du résumé
BACKGROUND
BACKGROUND
The adaptor protein Src homology 3 domain-binding protein 2 (SH3BP2) is widely expressed in immune cells. It controls intracellular signaling pathways. The present study was undertaken to investigate the role of SH3BP2 in a murine systemic lupus erythematosus model.
METHODS
METHODS
For the lupus model, we used
RESULTS
RESULTS
SH3BP2 deficiency significantly reduced lupus-like phenotypes, presented as splenomegaly, renal involvement, elevated serum anti-dsDNA antibody, and increased splenic B220
CONCLUSIONS
CONCLUSIONS
SH3BP2 deficiency ameliorated lupus-like manifestations. Modulating SH3BP2 expression could thus provide a novel therapeutic approach to autoimmune diseases.
Identifiants
pubmed: 33920631
pii: ijms22084169
doi: 10.3390/ijms22084169
pmc: PMC8073120
pii:
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
Sh3bp2 protein, mouse
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : JSPS KAKENHI
ID : 18K08398
Organisme : Foundation for the National Institutes of Health
ID : R01DE025870 and R21AR070953
Organisme : Research Project Grants from Kawasaki Medical School
ID : R02G-008, R01B-061, and 30G-005
Organisme : the KAWASAKI Foundation for Medical Science and Medical Welfare
ID : N.A.
Organisme : Japan Rheumatism foundation
ID : N.A.
Organisme : GSK Japan Research Grant
ID : N.A.
Organisme : UCB Japan
ID : N.A.
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