Figure 4.

Loss of sGSN permits tumor control dependent on CD8⁺ T cells

(A–E) Quantification of the indicated immune cell populations in the TME of B16 LA-OVA tumors growing in WT (n = 9) or sGsn^−/− (n = 10) mice at day 14 post-inoculation. Data are mean of frequency (%) of CD45⁺ cells (top) or the numbers of cells per gram of tumor (bottom) and are representative of two independent experiments.

(F) Quantification of intra-tumoral CD8⁺ OVA-specific pentamer⁺ cells at day 16 following subcutaneous inoculation of 0.3 × 10⁶ B16F10 cancer cells expressing LA-OVA-mCherry into WT (n = 9) or sGsn^−/− (n = 9) co-housed mice. Data are mean ± SEM of frequency of OVA-specific pentamer⁺ (% of CD3⁺ CD8⁺) cells (left) or the number of CD8⁺ OVA-pentamer⁺ cells per gram of tumor (right) and are representative of two experiments.

(G) Growth profile of 0.3 × 10⁶ B16F10 cancer cells expressing LA-OVA-mCherry implanted in WT mice. Mice received 300 μg of isotype control or anti-CD8 i.p. (days −3, 1, 4, 7, 10, 13). WT + isotype (n = 10) and WT + anti-CD8 (n = 10).

(H) As in (G) but using sGsn^−/− mice and comparing to an untreated WT group. WT (n = 21), sGsn^−/− + isotype (n = 10) and sGsn^−/− + anti-CD8 (n = 10).

Groups in (A–F) were compared using two-tailed unpaired t test with Welch’s correction. Tumor growth profiles (G and H) were compared using Bonferroni-corrected two-way ANOVA. ^∗p ≤ 0.05, ^∗∗p < 0.01, ^∗∗∗∗p < 0.0001; ns, not significant. See also Figure S4.