MONTREAL — The immune system has a self-destruct switch. Cancer cells have learned to flip it. And for years, doctors have been trying to jam that switch open.
Now a team at the Montreal Clinical Research Institute has found a second switch — one that works in a way nobody expected.
Dr. André Veillette, a medical professor at the Université de Montréal, published findings Wednesday in the journal Nature that identify a molecule called SLAMF6 on the surface of immune cells. This molecule, the team discovered, can suppress T cells — the body’s frontline cancer fighters — without needing any tumor signal to do so. It activates itself.
That is new. That is the problem.
Current immunotherapies — the PD1 and PDL1 inhibitors that have transformed cancer care in the last decade — rip away the brakes that tumors clamp onto immune cells. For many patients, that works. For a significant number, it does not. Some never respond. Some respond, then relapse. Their T cells stay quiet even after the main brake line is cut.
SLAMF6 is why.
This molecule sits on the T cell’s surface and binds to another copy of itself on the same cell. That self-binding sends a signal that weakens the immune attack. It is a self-contained suppressor. No tumor involvement required. It operates on its own.
That makes it a stubborn obstacle. Remove every tumor-driven inhibitor you want. SLAMF6 keeps working.
Veillette’s team did not just identify the problem. They built a tool to solve it. They created monoclonal antibodies designed to stop SLAMF6 from binding to itself. In laboratory tests, those antibodies blocked the suppressive signal. T cells stayed active.
The findings are still in the lab. They have not been tested in humans. But the researchers believe these antibodies could become the basis of a new cancer treatment — one aimed at patients who have run out of options.
The stakes are concrete. Cancer immunotherapy has been a revolution, but it is an incomplete one. A large fraction of patients gain no lasting benefit. The tumors that kill them are often the ones that figured out how to keep T cells suppressed even when the main inhibitory pathways are gone. SLAMF6 offers one explanation for that failure. And the antibodies offer one way around it.
Veillette and his team at IRCM have been studying SLAMF6 for years. This is not a side project. It is the central question of their work: what else is holding the immune system back? They found one answer.
There may be others. But for now, the discovery gives researchers a new target. A new molecule to block. A new mechanism to exploit.
For patients who have watched their tumors shrink on an immunotherapy drug, only to watch them grow back, this matters. For patients who never saw a response at all, this matters. The next generation of cancer treatments may not replace PD1 inhibitors. It may add to them. Block the first brake. Block this second one. Keep the immune system fighting.
That is the goal. The lab results say it is possible. The next step is proving it in people.
