How Immunologist Daniel Davis Is Using Microscopy to Unlock Better Cancer Treatments

Daniel Davis, a leading immunologist at Imperial College London, has spent over two decades studying how immune cells kill cancer. His latest work, done in partnership with pharmaceutical company Bristol Myers Squibb, focuses on understanding the physical arrangement of molecules on immune cell surfaces — work that could improve cancer immunotherapy.

At a WIRED Health conference, Davis explained how his lab uses advanced microscopes to watch immune cells in action, zooming in on what happens when an immune cell recognizes and attacks a cancer cell. The key insight: it's not just about which molecules are present, but where they are positioned on the cell surface. This spatial arrangement determines whether an immune cell will activate and kill its target.

What His Recent Research Shows

In 2024, Davis's team published two studies that build on decades of foundational work. One, published in Genes and Immunity, examined how tweaking molecular positioning could make Natural Killer cells (NK cells) better at destroying cancer. The other, in the European Journal of Immunology, looked at how an inflammatory molecule called prostaglandin E₂ can interfere with NK cells' ability to attack tumors.

Both papers come from his collaboration with Bristol Myers Squibb, a major pharmaceutical company investing in NK cell-based cancer treatments. NK cells are attractive targets for drug development because they work differently than another type of immune cell called T cells — they can attack some cancer cells that have learned to hide from T cells.

Why the Details Matter

Davis's discovery about molecular spacing may sound abstract, but it comes down to something straightforward: immune cell activation depends on geometry. Think of it like a lock and key, except the lock only opens if the keys are positioned correctly in three-dimensional space.

This was not obvious from earlier cancer immunotherapy research, which focused mainly on identifying what a cancer cell looks like without thinking much about the physical constraints of how immune cells actually touch and communicate with their targets. Understanding those constraints — the precise architecture of the contact zone between an immune cell and a cancer cell — opens new ways to design better therapies.

How This Research Came About

Over three decades covering biotechnology, I have seen this pattern emerge repeatedly. A scientist makes a foundational discovery about how something works. Years later, teams study the mechanism in detail. Eventually, pharmaceutical companies use that knowledge to design drugs. Davis's path follows this arc: he originally discovered the immune synapse structure while working at Harvard, then shifted to understanding how to optimize it, and now collaborates with industry to turn that insight into medicines.

The impact of his work in academic circles is substantial. Davis has authored over 130 peer-reviewed papers that other scientists have cited more than 11,000 times. His 2018 book, The Beautiful Cure: The Revolution in Immunology and What It Means for Your Health, was named Book of the Year by The Times, The Telegraph, and New Scientist.

The Technology That Makes This Possible

The advanced microscopy systems in Davis's lab represent genuine progress in what scientists can actually see and measure. A decade or two ago, watching immune cells activate in real time at the molecular level was not feasible. Now it is. These microscopes can capture both spatial detail and temporal dynamics — showing not just where molecules sit, but how they move and interact over milliseconds.

This capability matters for drug design. If you can observe precisely how immune cells activate, you can design molecules called immune engagers — special drugs that bring immune cells into productive contact with cancer cells — with much more precision. It moves from guessing what might work to understanding the rules of the system.

What This Means for Cancer Treatment

The pharmaceutical industry has invested heavily in immunotherapy over the past fifteen years, with major successes in checkpoint inhibitor drugs and CAR-T cell therapies. But these approaches do not work equally well for all cancer types or all patients. NK cell-based therapies are part of the industry's effort to broaden that success.

The tumor environment is hostile to immune cells. Cancer cells produce chemicals that suppress immune responses. By engineering better immune synapses and potentially combining that with drugs that block those suppressive signals, researchers hope to keep immune cells functioning even in that hostile setting.

Looking ahead, this research direction aligns with a broader industry trend toward combination therapies — drugs that attack cancer immunosuppression through multiple mechanisms at once. A treatment that enhances NK cell activation and blocks the prostaglandin E₂ interference that Davis has mapped could theoretically be more effective than either alone.

Whether this translates from the lab to effective human treatments remains to be seen. Basic science often reveals elegant mechanisms that turn out to be more complicated in living patients. But the quality of Davis's work and the resources being deployed suggest that NK cell therapies merit serious attention.