Francis Crick Institute press release
Under strict embargo: 10:00hrs BST Wednesday May 20, 2026
Peer reviewed
Experimental study
Cells and animals
- New research from the Francis Crick Institute and Adendra Therapeutics shows that immune cells can be redirected to recognise cancer by exploiting F‑actin, a structural protein exposed when tumour cells die.
- The findings point to new strategies to boost anti‑tumour immunity by expanding the pool of immune cells can recognise cancer cells and present cancer antigens.
As tumours outgrow their blood and nutrient supplies, or respond to treatments like chemotherapy and radiotherapy, individual cancer cells die, exposing their internal scaffolds. These dead cells are an abundant source of mutated proteins, or antigens, that can mark cancer cells as different from healthy ones. This is exactly what the immune system needs to recognise a tumour.
But a persistent puzzle in immunology is that many cancers remain poorly recognised by the immune system despite carrying large numbers of potentially visible antigens.
As Caetano Reis e Sousa, head of the Immunobiology Laboratory at the Crick, explains, “This reveals a blind spot in cancer immunity, where antigen presence alone is not enough to trigger an effective response.”
Caetano’s team have previously shown how specialised immune cells called dendritic cells can detect cancer cells after components of their internal scaffold become exposed. But only a very small proportion of immune cells have this ability - type 1 conventional dendritic cells (cDC1s) are particularly effective at capturing material from dead cancer cells and presenting it to T cells.
Overcoming the blind spot
In their latest study, published in Nature Cancer, the team have leveraged this understanding to promote anti-cancer immunity by redirecting other, more abundant immune cells to take on the same role.
Tom Castro Dopico, a Postdoctoral Fellow in the lab, developed biological reagents that link F‑actin from the scaffolding of dead cancer cells to receptors on nearby immune cells, effectively rerouting how this material is handled and triggering a T‑cell response against the tumour.
“When we tested this approach in mice, these antibodies effectively redirected non‑specialised immune cells to present a broader range of tumour antigens, leading to reduced tumour growth,” he describes. “This effect was strongest when combined with chemotherapy or radiotherapy, which increase the amount of dead tumour material, and therefore exposed F‑actin.”
Implications for immunotherapy
For Caetano, addressing this blind spot opens new avenues for developing immunotherapy treatments that complement existing clinical approaches. “We’re interested in how therapies might be refined by paying closer attention to what dying cells leave behind,” he adds. “Treatments such as chemotherapy and radiotherapy already create large amounts of tumour debris. By training the immune system to handle this material differently, we hope to amplify responses to tumours that would otherwise remain hidden.”
In 2021, Caetano co-founded Adendra Therapeutics to explore this opportunity further. Armed with this fresh insight into dendritic cell biology and a route to reshaping how the immune system sees cancer, the challenge is now to further refine anti F-actin reagents such as antibodies for safe use in people, and test whether they can trigger a consistent and lasting response in patients.
Raj Mehta, co-founder and CEO of Adendra Therapeutics, said: “These results are exciting because they confirm that much of what is currently ignored by the immune system in cancer can be redirected to enhance anti-tumour immunity.
Broadening of immune to tumour antigens has been shown to be required for efficacy of most immunotherapy approaches for treatment of cancer. Cross training non-cDC1 cells to enhance epitope spreading presents an opportunity to develop highly targeted immunotherapy treatments as single agents or in combination with other immune mediated therapies.
-ENDS-
For further information, contact: press@crick.ac.uk or +44 (0)20 3796 5252
Notes to Editors
Reference: Castro-Dopico et al. (2026). Coupling dead cell recognition to Fcγ receptors augments anti-cancer immunity. Nature Cancer. DOI: 10.1038/s43018-026-01168-5.
The Francis Crick Institute is a biomedical discovery institute dedicated to understanding the fundamental biology underlying health and disease. Its work is helping to understand why disease develops and to translate discoveries into new ways to prevent, diagnose and treat illnesses such as cancer, heart disease, stroke, infections, and neurodegenerative diseases.
An independent organisation, its founding partners are the Medical Research Council (MRC), Cancer Research UK, Wellcome, UCL (University College London), Imperial College London and King’s College London.
The Crick was formed in 2015, and in 2016 it moved into a brand new state-of-the-art building in central London which brings together 1500 scientists and support staff working collaboratively across disciplines, making it the biggest biomedical research facility under a single roof in Europe.
http://crick.ac.uk/http://crick.ac.uk/
Journal
Nature Cancer