Fig. 6∣. Anti-LILRB3 antibody ameliorates cancer development in vivo.

(a-b) Tumor progression of LILRB3 transgenic mice challenged with 5X10⁵ B16 melanoma cells (a) or MC38 colon cancer cells (b) and treated with either hIgG control or anti-LILRB3. (c) Representative Western blot of B16 and MC38 whole cell lysates for mouse galectin-4, vinculin loading control, and mouse galectin-7. (d) Percentages of LILRB3 reporter cells activated on coated mouse galectin-4 (20 μg/mL) with hIgG control or anti-LILRB3 (20 μg/mL). (e) Tumor progression of LILRB3 transgenic mice challenged with 5X10⁵ MC38-hGal4 and treated with hIgG control or anti-LILRB3, and a combination of anti-CD4 and anti-CD8 or isotype control. (f-g) Quantification of proliferating mouse CD4⁺ (f) or CD8⁺ (g) T cells cocultured with MDSCs from B16-challenged LILRB3 transgenic mice. Cocultured cells were treated with hIgG control or anti-LILRB3 (20 μg/mL). (h-i) Quantification of proliferating mouse CD4⁺ (h) or CD8⁺ (i) T cells cocultured with naïve Mac1⁺Gr1⁺ cells from unchallenged LILRB3 transgenic mice on coated human galectin-4 or BSA (10 μg/mL) and treated with hIgG control or anti-LILRB3 (20 μg/mL). Three technical replicates were performed for each condition and at least two independent experiments were performed for each condition. Error bars represent SEM and * indicates two-tailed student’s t-test p < 0.05. *** indicates two-tailed student’s t-test p < 0.0005.