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Long-lasting mRNA-encoded interleukin-2 restores CD8 - Cell Press
2024年3月14日 · In CT26-B2m −/− and MC38-B2m −/− tumors, expression of Il2, which promotes proliferation of immune cells, and Ifng, an effector molecule released by CD8 + T cells upon cognate antigen recognition, were significantly reduced (Figure 1F).
Different syngeneic tumors show distinctive intrinsic tumor …
2022年2月28日 · In three syngeneic tumors (MC38, CT26 and EMT6) where CD8 +-CTL-TILs seem to be directly responsible for anti-PD-1 mediated tumor inhibition, CD8 +-TIL depletion combined with anti-PD-1...
ID1 expressing macrophages support cancer cell stemness and limit CD8
2023年11月23日 · ID1 expressing macrophages maintain cancer stemness and impede CD8 + T cell infiltration. Mechanistically, ID1 interacts with STAT1 to induce its cytoplasmic distribution and inhibits...
Antibody-mediated targeting of TNFR2 activates CD8 - Science
Presently, we show that Y9 activates both CD8 + and CD4 + T cells in vitro, and that Y9 loses activity in the CT26 model when these cell types are depleted. In addition, NK cells were also implicated in the activity of Y9 in vivo.
JITC:南京大学团队整合两种免疫疗法,重构肿瘤微环境! - 专区
2022年1月16日 · CT26是一种免疫原性相对较高的肿瘤模型,VV-scFV-TIGIT对其疗效较为理想,那么,在T淋巴细胞浸润较少,肿瘤微环境抑制性更强的“冷” 肿瘤 ——H22 肝癌 腹水 肿瘤 模型中,VV-scFV-TIGIT是否又能大显神通呢? 令人欣喜的是,在H22腹水肿瘤模型中,腹腔注射VV-scFV-TIGIT后,肿瘤细胞比例降低,淋巴细胞浸润增加,除此以外, 肿瘤 浸润免疫细胞的杀伤性也有所提高,荷瘤小鼠的生存率也提高了。 无论是对CT26结肠癌 肿瘤 还是H22 肝癌 肿 …
Cancer-Cell-Intrinsic cGAS Expression Mediates Tumor Immunogenicity
2019年10月29日 · Depletion of CD8 + T cells promoted the growth of CT26 ctrl, but not CT26 ΔMb21d1, tumors (Figure S2K). This underscores the relevance of CD8 + T cells for controlling CT26 tumor growth as well as the importance of cancer-cell-intrinsic cGAS for recruiting those T cells (Figure 2E).
Immunotherapy of CT26 murine tumors is ... - Wiley Online Library
2020年5月29日 · Our data suggest that successful immunotherapy of CT26 tumors requires an oligoclonal expansion of functional tumor-specific tissue-resident memory CD8 + T cells (T RM) and that a relatively small number of lymphocyte specificities drive the tumor rejection process.
CCL5-deficiency enhances intratumoral infiltration of CD8
2018年7月10日 · Here, we demonstrated that CCL5-deficiency delayed tumor growth and metastasis via facilitating CD8 + T cells to accumulate into tumor site in CRC mouse models. Furthermore, CCL5-deficiency could...
Tumor-immune profiling of CT-26 and Colon 26 syngeneic mouse …
2021年11月13日 · We hypothesized that anti-PD-1 mediated tumor growth inhibition in CT-26 model was due to enhanced frequency of PD-1-expresing CD8 T cells within the tumor. As shown in Fig. 2I, CT-26 tumors at baseline have higher frequency of PD-1
VEGF-A modulates expression of inhibitory checkpoints on CD8
We first analyzed the impact of VEGF-A–VEGFR blockade on PD-1 expression on tumor-infiltrating CD8 + T cells in a mouse model of colorectal cancer (CT26). CT26 tumor cells produce high levels of VEGF-A in vitro (Terme et al., 2013). In vivo, the VEGF-A concentration was ∼10 times higher in the tumor microenvironment, reaching 366.9 ± 53.8 ...