A collaborative study has discovered a new immune checkpoint that may be exploited for cancer therapy. The study shows that by inhibiting the protein tyrosine phosphatase PTP1B in T cells, the body’s immune response to cancer can be mobilized, helping to repress tumor growth.

The study shows that by inhibiting the protein tyrosine phosphatase PTP1B in T cells, the body’s immune response to cancer can be mobilised, helping to repress tumour growth.

T cells are an essential part of the body’s immune system, helping not only to kill invading pathogens, such as viruses but also cancer cells. However, this study has shown that using a new drug candidate, the abundance of PTP1B in T cells that infiltrate tumours is increased, thereby restraining the ability of T cells to attack tumour cells and combat cancer. These findings have identified PTP1B as an intracellular brake, or checkpoint, reminiscent of the cell surface checkpoint PD-1 — the blockade of which has revolutionised cancer therapy.

The findings are published in the journal Cancer Discovery.

Using mice, scientists from Monash BDI, in conjunction with colleagues at the Peter MacCallum Cancer Centre in Melbourne and Cold Spring Harbor Laboratory in New York, found that by inhibiting PTP1B, using an early-stage injectable drug candidate that has previously been shown to be safe and well-tolerated in humans, the cancer-fighting ability of T cells is enhanced, repressing tumour growth.

Remarkably, the authors showed that the inhibition of this intracellular checkpoint, PTP1B, can also enhance the response to a widely used cancer therapy that blocks the PD-1 checkpoint on the surface of T cells.

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