Figure 6
Figure 6. BCR triggering increases chemotaxis of CLL cells toward CXCL12 and CXCL13. (A) CLL cells from 15 different patients were assayed for chemotaxis toward CXCL12 (▩) or CXCL13 (■) after incubation for 48 hours without (control) or with anti-IgM. Displayed is the mean relative chemotaxis (± SEM, n = 15) of anti-IgM–stimulated CLL cells, compared with unstimulated controls (100%). Anti-IgM treatment significantly increased CLL cell chemotaxis toward both CXCL12 and CXCL13, with P < .05, as indicated by the asterisks. (B-C) Displayed are scatter dot plots that represent the relative chemotaxis of 15 CLL samples after 48 hours of treatment with anti-IgM in ZAP-70–positive CLL samples (●, n = 9) and ZAP-70–negative CLL samples (○, n = 6) toward CXCL12 (B) or CXCL13 (C). Enhanced chemotaxis after anti-IgM treatment was more apparent in ZAP-70–positive samples; however, this difference between ZAP-70–positive and ZAP-70–negative CLL samples was significant only for CXCL12 (P < .05).

BCR triggering increases chemotaxis of CLL cells toward CXCL12 and CXCL13. (A) CLL cells from 15 different patients were assayed for chemotaxis toward CXCL12 (▩) or CXCL13 (■) after incubation for 48 hours without (control) or with anti-IgM. Displayed is the mean relative chemotaxis (± SEM, n = 15) of anti-IgM–stimulated CLL cells, compared with unstimulated controls (100%). Anti-IgM treatment significantly increased CLL cell chemotaxis toward both CXCL12 and CXCL13, with P < .05, as indicated by the asterisks. (B-C) Displayed are scatter dot plots that represent the relative chemotaxis of 15 CLL samples after 48 hours of treatment with anti-IgM in ZAP-70–positive CLL samples (●, n = 9) and ZAP-70–negative CLL samples (○, n = 6) toward CXCL12 (B) or CXCL13 (C). Enhanced chemotaxis after anti-IgM treatment was more apparent in ZAP-70–positive samples; however, this difference between ZAP-70–positive and ZAP-70–negative CLL samples was significant only for CXCL12 (P < .05).

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