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http://purl.uniprot.org/citations/19866343http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Introduction

Aberrant signaling within and between B and T cells, considered to be central in systemic lupus erythematosus (SLE), could depend on enhanced CD40-CD154 activation. As a result, autoreactive B cells, normally anergic, differentiate and secrete antibodies attacking several normal tissues. Thus restorating B cell homeostasis might help control this disease. In this study, two facets of SLE B cells were investigated, namely their in vitro response to CD40-CD154 and the effect of treatment with human immunoglobulins for intravenous use (IVIg).

Materials and methods

Blood samples from SLE patients and healthy volunteers were obtained and used to isolate B cells, which were activated through CD40 in the presence or absence of IVIg. The phenotype, proliferation, and differentiation of the SLE B cells were determined and compared with those of control B cells using flow cytometry and standard ELISA.

Results

In this model, CD40-activated SLE B cells, as control B cells, proliferated and differentiated and were characterized by the emergence of CD19(lo)CD38(++)CD138(+)CD27(++) cells. IVIg treatment of the CD40-activated SLE B cells resulted in higher differentiation, characterized by increased secretion rates of IgG and IgM, as reported previously for control B cells.

Conclusions

Taken as a whole, such accelerated differentiation of CD40-activated B cells suggests that IVIg may participate in re-equilibration of the antibody repertoire by replacing pathological antibodies by de novo harmless antibodies."xsd:string
http://purl.uniprot.org/citations/19866343http://purl.org/dc/terms/identifier"doi:10.1007/s00005-009-0048-3"xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/author"Cote S."xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/author"Jacques A."xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/author"Boire G."xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/author"Neron S."xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/author"Racine C."xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/author"de Brum-Fernandes A.J."xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/author"Dussault N."xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/name"Arch Immunol Ther Exp (Warsz)"xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/pages"447-458"xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/title"CD40-activated B cells from patients with systemic lupus erythematosus can be modulated by therapeutic immunoglobulins in vitro."xsd:string
http://purl.uniprot.org/citations/19866343http://purl.uniprot.org/core/volume"57"xsd:string
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