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A team from the University of Oxford has visualised how key cells of the immune system lock onto cancerous or infected cells to destroy them. The work was led by the Mike Dustin’s group at the Kennedy Institute of Rheumatology and experts in colorectal and ovarian cancers from across Oxford and computational biologists at the University of Birmingham.

T cell © Shutterstock

CD2 was one of the first molecules to be identified on the surface of T cells. The connection of thousands of molecules of CD2 on T cells to thousands of CD58 molecules on target cells facilitates destruction of cancerous and infected targets. The new work, published in Nature Immunology shows how the exact number of these molecular connections controls the process and how reductions of these numbers may undermine the immune response to cancer.

Dustin’s team first investigated the number of CD2 molecules on T cells controls the efficiency of T cell sensing of potential targets through a striking ‘CD2 corolla’, which they could visualize using advanced microscopy.  They then found that the T cells responsible for cancer killing had lower numbers of CD2 molecules in most colorectal and ovarian tumours that needed to be removed surgically.  The inability of the patients T cells to form the CD2 corolla in the tumour may have contributed to disease progression. 

Lead author Professor Michael Dustin, of the Kennedy Institute said: “Understanding why the potentially lifesaving T cells have low CD2 in tumours may help us understand why the immune system sometimes fails to control cancer and how we might help the patient's immune system fight cancer better by boosting CD2 expression.”

The findings also provide a framework to interpret the significance of CD2 expression in different contexts and the role it plays in disease.

The full story is available on the Nuffield Department of Orthopaedics, Rheumatology & Musculoskeletal Sciences website

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