Complement Receptor Type 1 Suppresses Human B Cell Functions in SLE Patients

Figure 3

Impact of CR1 clustering on BCR-induced plasmablast formation (a–c) and IgM secretion (d-e) of human B cells. 2 × 10⁵ B cells isolated from healthy donors (a and d) or active SLE patients (b and e) were activated for 6 days with the F(ab’)₂ fragment of anti-human IgG+M+A Ab (5 μg/mL) in the presence of 50 ng/mL IL-10, IL-2, and IL-6 and treated with different concentrations of heat-aggregated C3. (a and b) The percentage of plasmablasts was determined at day 6 by flow cytometry. Data show mean frequency of cells ± SD of duplicate samples. One representative experiment of six is shown. (d and e) Supernatants of cultured cells were collected on day 6 and were measured for secreted IgM by reverse phase protein microarray. Data are expressed as mean ± SD relative fluorescence intensity of triplicate measurements. Results are representative of six independent experiments in the case of both healthy donors (d) and active SLE patients (e). (c and f) Results showing percent of inhibition mediated by aggregated C3 are mean % of inhibition ± SEM of six independent experiments and correlated with the CR1-agonist untreated sample (see Section 2, Permutation-test; and ).

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