[The abnormality of FcgammaRIIB1-mediated signaling and the hyperactivity of B cells from patients with systemic lupus erythematosus].
OBJECTIVE
To evaluate the effect of FcgammaRIIB(1) (CD32) representative self-inhibitory adjustive mechanism of B cells on pathogenesis of systemic lupus erythematosus (SLE) by observing the expression characteristic and functional state of molecules on the surface of B cells from SLE patients.


METHODS
The peripheral blood mononuclear cells (PBMC) were prepared by density gradient centrifugation, and the B cells were isolated from PBMC by magnetic activated cell sorting (MACS). The fluxes of intracytoplasmic calcium ([Ca(2+)](i)) of B cells activated by different activators were measured by fluorescence spectrophotometric method. The IgG production by B cells cultured with activators was assayed by ELISA. The expression levels of CD32, CD19, and IgM on the surface of B cells were measured by flow cytometry.


RESULTS
(1)After B cells were stimulated with goat anti-human mu chain F(ab')(2) fragments and whole IgG respectively, the ratio of [Ca(2+)](i) response by F(ab')(2) fragments to whole IgG was significantly lower in SLE B cells compared to rheumatoid arthritis (RA)(P<0.05) or normal (P<0.01) B cells. (2)The ratio of total IgG production by B cells cultured with staphylococcal protein A (SPA) to SPA plus IgG anti-mu chain was significantly lower in SLE patients compared to RA patients or normal individuals (P<0.05). (3)There was no obvious difference in the expression of CD19, CD32, and IgM on the surface of B cells from SLE, RA patients and normal individuals (P>0.05).


CONCLUSIONS
The inhibitory signaling abnormality of CD32 possibly contributes to the mechanism of hyperactivity of human SLE B cells.
Peng
Ke-Jun
KJ
Department of Laboratory Medicine, Chengdu Medical College, Chengdu 610083, China. pengkejungym@163.com
Xiao
Lin-Sheng
LS
Fei
Ying
Y
Wang
Shu-Ren
SR
D000328:Adult; D000818:Animals; D018941:Antigens, CD19 / Q000378:metabolism; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D002118:Calcium / Q000378:metabolism; D016022:Case-Control Studies; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D007075:Immunoglobulin M / Q000378:metabolism; D007148:Immunoglobulin mu-Chains / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D008297:Male; D017452:Receptors, IgG / Q000276:immunology / Q000378:metabolism*; D015398:Signal Transduction
D018941:Antigens, CD19; C080571:Fc gamma receptor IIB; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007148:Immunoglobulin mu-Chains; D017452:Receptors, IgG; D002118:Calcium