Cancer Discovery: Novel immune checkpoint: can be used to enhance T cells against cancer, and also allows CAR-T to fight solid tumors

T cells are an important part of the body's immune system, helping not only to clear invading pathogens, such as viruses, but also to kill cancer cells

In recent years, cellular immunotherapy, represented by CAR-T, transforms T cells of cancer patients in vitro to make them recognize antigens on the surface of tumor cells, and then infuse these cells back into the patient to recognize and kill cancer cells the therapeutic effect

Immune checkpoint therapy represented by PD-1/PD-L1 inhibitors is considered to have completely changed the cancer treatment landscape and has a good therapeutic effect on a variety of cancers, but not all patients respond, and with As treatment progresses, drug resistance emerges

Recently, researchers from Monash University in Australia published a research paper entitled: PTP1B Is an Intracellular Checkpoint that Limits T-cell and CAR T-cell Antitumor Immunity in the journal Cancer Discovery .

The study found that inhibiting protein tyrosine phosphatase 1B (PTP1B) on T cells mobilized the body's immune response to cancer and helped suppress tumor growth

This study identified PTP1B as an intracellular immune checkpoint and a cancer therapeutic target.

In this study, the research team found that high expression of PTP1B on T cells restricted T cell expansion and inhibited its cytotoxic effects, thereby promoting tumor growth

Next, the research team conducted validation experiments in mouse models and found that inhibiting PTP1B enhanced the cancer cell's response to PD-1 inhibitors

To advance this work, the research team said, a critical next step will be to further determine the impact of PTP1B loss on human CAR-T and conventional T cells

The research team will collaborate with DepYmed, which develops PTP1B inhibitors, to pool and test the effects of oral PTP1B inhibitors in preclinical animal models, laying the foundation for future clinical trials

Original source:

Florian Wiede, et al.