Skip to main content
Fig. 1 | Journal of Hematology & Oncology

Fig. 1

From: Antibody targeting tumor-derived soluble NKG2D ligand sMIC reprograms NK cell homeostatic survival and function and enhances melanoma response to PDL1 blockade therapy

Fig. 1

sMIC compromises tumor response to anti-PDL1 mAb therapy and that antibody targeting sMIC generates cooperative therapeutic effect with anti-PDL1 mAb. a Depict of the therapy. B16F10 or sMICB-expressing B16F10-sMICB cells (4 × 105 cells/mouse) were s.c. injected into syngeneic MICB/B6 host. Therapy initiated when tumors reached a volume of 75–100 mm3. Antibody (3 mg/kg) was given i.p. twice weekly till designated study endpoint as specified in the “Materials and methods” section. b, c Therapeutic response of B16F10 (b) and B16F10-sMICB (c) tumors to anti-PDL1 therapy. Data showed a compromised response of B16F10-sMICB tumors to anti-PDL1 therapy. d B16F10-sMICB tumor growth curve in response to sMIC-targeting antibodyB10G5 and anti-PDL1 antibody single-agent therapy and combination therapy. e Kaplan-Meier survival curve showing that B10G5 and anti-PDL1 combination therapy significantly prolonged survival of mice bearing B16F10-sMICB tumors. Note that tumor volume of 1800 mm3 was designated as survival endpoint. N = 5–7 per group, *p < 0.05; **p < 0.01

Back to article page