2024年11月5日 · We injected syngeneic hosts with B16-F10 melanoma expressing OVA (B16-OVA), then transferred OTI or OTI/LDH-A-/-T cells and monitored tumor growth. Strikingly, we found significantly larger tumors, a higher CD4/8 T cell ratio, and less CD8 + T cell infiltration in recipients of OTI/LDH-A-/-T cells.

2024年9月3日 · In B16 melanoma and MC38 colon cancer, LDH inhibition resulted in increased glucose-uptake capacity in all 3 T cell subtypes, suggesting potentiation of antitumor Teff function and reduction of Treg-mediated immunosuppression. Our results further emphasize the importance of intratumoral glucose availability in modulating T cell responses.

2018年10月12日 · To elucidate the role of LDHA in tumors, we knocked out the LDHA gene in two glycolytic cancer cell lines, human colon adenocarcinoma (LS174T) and mouse melanoma (B16-F10) cells (Fig. 1, A and C), using the CRISPR-Cas9 technique (densitometric quantification of the corresponding Western blots is presented in Fig. 1, B and D).

In this study, we investigated the role of LDH-A expressed in tumors for modulating immune responses to anti-PD-1 therapy in a B16-F10 melanoma model. We hypothesized that PD-1 blockade using an anti-PD-1 antibody might further inhibit the effects of the remaining PD-L1 expressed on tumor cells and block PD-1 signaling on immune cells.

2023年11月17日 · 作者发现usp22敲低增强了ldh释放，表明b16-f10细胞中t细胞介导的细胞杀伤升高，而同时异位表达pd-l1以某种方式恢复了这种效应。 根据KMpoltter数据库，低USP22基因表达与肺癌患者更好的预后相关。

6 天之前 · Whereas control cells were not susceptible to IFNγ-induced cell death, VDAC2-deficient B16-OVA cells showed markedly increased cell death and lactate dehydrogenase (LDH) release after IFNγ (but ...

2024年11月5日 · We injected syngeneic hosts with B16-F10 melanoma expressing OVA (B16-OVA), then transferred OTI or OTI/LDH-A-/-T cells and monitored tumor growth. Strikingly, we found significantly larger tumors, a higher CD4/8 T cell ratio, and less CD8 + T cell infiltration in recipients of OTI/LDH-A -/- T cells.

In line with LDH-mediated lactate secretion and acidification as a resistance mechanism to immune checkpoint therapy, combined treatment with anti-PD-1 and anti-CTLA-4 antibodies resulted in a long-term growth control of B16 LDH −/− tumors (Figure 6N).

To investigate whether lowering LDH activity could reprogram CD8 + T cell function, we used a mouse model of adoptive cancer immunotherapy in which pmel-1 CD8 + T cells recognizing the melanoma-melanocyte differentiation antigen gp100 were transferred into C57BL/6 mice bearing subcutaneous B16 melanoma expressing the mutated gp100 antigen B16 ...

To elucidate the role of LDHA in tumors, we knocked out the LDHA gene in two glycolytic cancer cell lines, human colon adenocarcinoma (LS174T) and mouse melanoma (B16-F10) cells (Fig. 1, A and C), using the CRISPR-Cas9 technique (densitometric quantification of the corresponding Western blots is presented in Fig. 1, B and D).