A statistical test based on measures of central tendency comparison was not applicable to the particular case of anti-IgM combined with IL-21. A P-value less than 0·05 was considered statistically significant. B cells die from apoptosis if maintained unstimulated in culture . After 3 days, spontaneous apoptosis was higher in CD27+ than in CD27– B cells (79·2 versus 57·6%, P < 0·001) (Fig. 2a). When B cells are stimulated, they are rescued from apoptosis.
The effectiveness of the rescue depends upon both the kind of stimulus used and the subpopulation of B cells. For CD27– B cells, the strongest rescue effect was induced by anti-CD40 followed by CpG-ODN and to a lesser extent by anti-IgM, whereas for CD27+ B cells, CpG-ODN appeared to be the strongest rescue stimulus (Fig. 2b). Nevertheless, all the stimuli evaluated were more efficient in the CD27– than in the CD27+ Angiogenesis chemical population: anti-CD40 (77·9 versus 23·9%, P < 0·001), CpG-ODN (71·4 versus Crenolanib mw 57·3%, P < 0·01) and anti-IgM (52·7 versus 36·9%; P < 0·01) (Fig. 2b). Proliferation was evaluated simultaneously. Anti-CD40 and anti-IgM did not induce proliferation of either CD27– or CD27+ B cells while CpG-ODN induced proliferation of both subpopulations (Table 2). Although CpG-ODN
induced a lower level of proliferation on CD27– than CD27+ B cells (PI = 0·1 versus PI = 1·8, respectively; P < 0·001) (Table 2), it induced higher rescue from apoptosis in the CD27– population (Fig. 2b). These aforementioned results suggest that proliferation and rescue from apoptosis are two independent processes. CD27– B cells from CVID MB0 patients were less sensitive to rescue from apoptosis when stimulated with a T-dependent stimulus (anti-CD40) than control subjects (65·4 versus 77·9%, P < 0·05)
(Fig. 3a). They were also less sensitive to rescue from apoptosis when stimulated with a T-independent stimulus (CpG-ODN) than control subjects or CVID MB1 patients, although differences did not reach statistical significance (58·8 versus 71·4 and 63·0%, respectively, P = 0·075). CD27– B cells from CVID MB1 patients were rescued from apoptosis similarly to controls, regardless of the stimulus used (Fig. 3a). After BCR engagement with anti-IgM CD27– B cells from both CVID MB0 and MB1, patients old were rescued equally from apoptosis than healthy controls. CD27+ B cells from CVID MB0 patients, stimulated with either a T-dependent (anti-CD40) or a T-independent stimulus (CpG-ODN), were less sensitive to apoptosis rescue than control subjects (6·0 versus 23·9%, P < 0·01; and 23·2 versus 57·3%, P < 0·05, respectively) and CVID MB1 patients (6·0 versus 30·6%, P < 0·001; and 23·2 versus 65·7%, P < 0·01, respectively). They were also less sensitive to rescue from apoptosis after BCR engagement with anti-IgM than control subjects (19·2 versus 36·9%, P < 0·05) or CVID MB1 patients (19·2 versus 38·2%, P < 0·01) (Fig. 3b).