Figure 7
Figure 7. In vivo anti-lymphoma activity by CD37-SMIP is dependent on NK cells. (A) Decreased ex vivo NK-cell activity in splenocytes from mice treated with anti-asialo GM1 antibody. Splenocytes from control or mice treated with NK-cell–depleting anti-asialo GM1 antibody were tested for their ability to mediate cytotoxicity against NK-cell target Yac-1 cells. Solid and broken lines represent percentage lysis mediated by cells from NK-undepleted and -depleted mice, respectively. (B) Depletion of NK cells reduced therapeutic efficacy of CD37-SMIP in vivo. In vivo therapeutic efficacy of trastuzumab, CD37-SMIP or rituximab were compared in control (NK+) or anti-asialo GM1 antibody–treated (NK−) Raji xenograft model. Survival is determined based on the paralysis time after inoculation. Log-rank test was applied for statistical analysis.

In vivo anti-lymphoma activity by CD37-SMIP is dependent on NK cells. (A) Decreased ex vivo NK-cell activity in splenocytes from mice treated with anti-asialo GM1 antibody. Splenocytes from control or mice treated with NK-cell–depleting anti-asialo GM1 antibody were tested for their ability to mediate cytotoxicity against NK-cell target Yac-1 cells. Solid and broken lines represent percentage lysis mediated by cells from NK-undepleted and -depleted mice, respectively. (B) Depletion of NK cells reduced therapeutic efficacy of CD37-SMIP in vivo. In vivo therapeutic efficacy of trastuzumab, CD37-SMIP or rituximab were compared in control (NK+) or anti-asialo GM1 antibody–treated (NK) Raji xenograft model. Survival is determined based on the paralysis time after inoculation. Log-rank test was applied for statistical analysis.

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