1. Autoantibody-producing RP105- B cells, from patients with systemic lupus erythematosus, showed more preferential expression of BCMA compared with BAFF-R than normal subjects
- Author
-
Mio Mitamura, Yoshio Haruta, Hiromi Ehara, Yoshifumi Tada, Kohei Nagasawa, Akihide Ohta, Syuichi Koarada, Rie Suematsu, Yusuke Tokoro, Hisako Inoue, and Yoshiaki Sohma
- Subjects
Adult ,Male ,medicine.medical_specialty ,Adolescent ,medicine.disease_cause ,Polymerase Chain Reaction ,Autoimmunity ,Flow cytometry ,Young Adult ,Rheumatology ,Antigen ,immune system diseases ,Internal medicine ,medicine ,Humans ,Lupus Erythematosus, Systemic ,Pharmacology (medical) ,B-Cell Maturation Antigen ,skin and connective tissue diseases ,BAFF receptor ,B-cell activating factor ,Aged ,Autoantibodies ,CD40 ,biology ,medicine.diagnostic_test ,business.industry ,Autoantibody ,Middle Aged ,Flow Cytometry ,Molecular biology ,Endocrinology ,Case-Control Studies ,biology.protein ,Female ,business ,B-Cell Activation Factor Receptor - Abstract
OBJECTIVE B cells lacking RP105 produce autoantibodies in patients with SLE. Expression of B-cell activating factor (BAFF) binding receptors (BBRs) and survival of RP105(-) B cells from SLE patients were examined. METHODS Detection of difference of gene expression between RP105(-) and RP105(+) B cells was done by DNA microarrays. Surface expression was confirmed by flow cytometry. The contribution of BAFF, a proliferation-inducing ligand (APRIL) and monomers/trimers of sCD40L to survival of RP105(-) and RP105(+) B cells was examined. RESULTS Gene expression of B-cell maturation antigen (BCMA) was different among BBRs in RP105(-) and RP105(+) B cells in SLE. Preferential expression of BCMA on RP105(-) B cells was confirmed compared with RP105(+) B cells by flow cytometry, although BAFF receptor (BAFF-R) expression on RP105(-) B cells was significantly lower. Additionally, relative ratios of BCMA/BAFF-R expression on RP105(-) B cells were increased significantly in SLE patients compared with normal subjects. Stimulation by sCD40L decreased the number of surviving RP105(-) and RP105(+) B cells in vitro. RP105(+) B cells were not rescued from sCD40L-induced cell death by BAFF and/or APRIL. In contrast, either BAFF or APRIL maintained the survival of RP105(-) B cells due to avoidance of cell death. Activated RP105(-) B cells reduced BAFF-R and increased BCMA levels. CONCLUSIONS RP105(-) B cells from SLE patients showed more preferential expression of BCMA compared with BAFF-R than normal subjects, and were possibly regulated by BAFF/APRIL. Our results provide a new insight of BCMA and their ligands in B cells from SLE patients.
- Published
- 2010