[The abnormality of FcgammaRIIB1-mediated signaling and the hyperactivity of B cells from patients with systemic lupus erythematosus].

AIM: To evaluate the effect of FcγRⅡB_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 μ 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 (P0.01) B cells. (2)The ratio of total IgG production by B cells cultured with staphylococcal protein A (SPA) to SPA plus IgG anti-μ chain was significantly lower in SLE patients compared to RA patients or normal individuals (P0.05). (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 (P0.05). CONCLUSION: The inhibitory signaling abnormality of CD32 possibly contributes to the mechanism of hyperactivity of human SLE B cells.