Anti-CD160 antibodies induce cell proliferation through PI3K activation. (A) MEC-I cells (105/mL) were cultured with isotype control (IgG or IgM) or anti-CD160 (CL1-R2 or BY55) mAb, (B) with or without the PI3K inhibitor LY294002, and the cells were counted after 72-hour incubation. Results are expressed as a percentage of basal control growth (ie, isotype control = 100%), and are representative of 3 independent experiments ± SEM. (A) *P = .02; **P = .01 (anti-CD160 vs isotype control). (B) *P = .036; **P = .029 (CL1-R2 plus LY294002 vs CL1-R2 alone). (C) CLL cells (2 × 105) were treated with isotype control (IgG or IgM) mAb and CL1-R2 or BY55. 3H-thymidine was added for the last 16 hours of a 72-hour incubation. Data are expressed as average percentage of basal growth (ie, isotype control = 100%) of 22 patients ± SEM, *P = .005, **P = .004 (anti-CD160 vs isotype control). (D) CLL cells were treated with isotype control mAb (IgG or IgM), CL1-R2, or Pan-Ig mAb (anti-IgG,M,A), all at a concentration of 10 μg/mL. 3H-thymidine was measured and analyzed as in panel C; the bars represent the mean values of 22 patients ± SEM; *P = .004, **P = .002 compared with control. (E) CLL cells were coincubated with control IgG or CL1-R2 and LY294002 for 24 hours and Ki67 expression was measured by flow cytometry. The data represent the mean ± SEM of 5 patients (*P = .002, **P = .001).
