Many breast cancers do not respond well to current immunotherapies. Our findings reveal a previously unrecognised mechanism by which immune cells within tumours are regulated. While CD1d is best known for helping immune cells recognise lipid molecules, we found that it also plays a role in shaping the behaviour of myeloid cells within tumours. These findings suggest that targeting the immune cells that surround and support tumours could boost anti-cancer immunity and potentially improve treatment responses in the future.
Professor Patricia Barral, Professor of Immunobiology at King’s College London and senior author of the paper
08 September 2026
Researchers identify potential target to boost anti-cancer immunity in breast cancer
Researchers have identified a potential target to make the environment surrounding breast tumours more favourable to anti-cancer immune responses.
The researchers found that reducing or blocking a molecule called CD1d changed the types and behaviour of immune cells found within tumours, slowing tumour growth and improving the response to immunotherapy in mouse models of breast cancer.
The findings, published in The Journal of Experimental Medicine, could pave the way for the development of new approaches to improve the effectiveness of immunotherapies for breast cancer.
Researchers from King’s College London, the Francis Crick Institute and University College London wanted to better understand how immune cells inside breast tumours influence cancer growth. They focused on myeloid cells, a group of immune cells that are abundant in tumours and can either help the immune system attack cancer or support tumour growth and immune evasion.
The team investigated the role of CD1d, a molecule found on the surface of myeloid and other immune and tissue cells that helps regulate the immune response. They found that when CD1d was genetically removed from cells in a mouse model of breast cancer, mice were more resistant to tumour growth and had distinct changes in the different myeloid cell populations within their tumours, including increased activity from cells that can help attack cancer.
To test the therapeutic potential of targeting CD1d, the researchers blocked its activity using an antibody. They saw changes in the myeloid cells present in tumours and slower tumour growth. CD1d blockade with the antibody also led to improved responses to immunotherapy in the mouse model. The findings suggest that reducing or blocking CD1d creates an environment that is more favourable for anti-cancer immunity.
To understand these changes in more detail, the researchers used single-cell RNA sequencing to examine the individual immune cells within CD1d-deficient tumours and identify changes in their gene activity. They saw that there was a population of myeloid cells, called monocytes, that expressed genes associated with inflammation – an important part of the immune response. These cells were particularly important for restricting tumour growth in the mouse models.
The team saw a similar gene expression pattern, or ‘gene signature,’ when they examined gene expression data from human breast cancer tumours. The presence of this gene signature in the myeloid cell populations in human tumours was found to be associated with positive responses to immunotherapy in breast cancer patients.
The next step for the researchers is to better understand how these immune changes occur and how they can be safely harnessed in patients. The researchers also want to explore whether targeting CD1d could enhance current treatments and potentially influence treatment response in different cancer types.
The work was supported by funding from the UKRI BBSRC, Breast Cancer Now and the Cancer Research UK City of London Centre.
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Professor of Immunobiology