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tumours put up a protein "smokescreen" to escape the body’s immune system, and blocking those proteins helps kill cancer cells in mice, a new study has found. the work also offers new insight into why some inflammatory diseases increase a person’s risk of cancer.
the immune-system protein that appears to help tumours escape attack is called cytokine interleukin 23 (il-23). high levels of il-23 were found in the human tumours studied by martin oft at the schering-plough institute in palo alto, california, us, and his colleagues. the team also found that mice deficient in il-23 did not develop as many tumours as normal mice.
under ordinary circumstances, il-23 contributes to the recruitment of cells known as neutrophils. these play an important role in the early immune response to an infection, targeting foreign particles in the body.
but the tough task of infiltrating diseased tissues and rooting out the source of an illness belongs to another kind of immune cell called cd8 t-cells, oft explains. and it is these cells that il-23 appears to repel. in the case of cancer, excess il-23 prevents the cd8 t-cells from eliminating a tumour.
in one part of the experiment, mice received an antibody molecule that blocks il-23. these animals developed fewer tumours and eliminated injected cancer cells more quickly than control mice. the researchers think the antibody holds promise as a future tool to fight cancer in humans, but they stress that it remains in the pre-clinical phase of development.
the team's work also addresses the link between chronic inflammation and cancer, which doctors have suspected for more than a century. for example. some inflammatory illnesses – such as psoriasis and inflammatory bowl disease – are associated with an increased cancer risk.
the team's work explains this link because earlier work has shown that excess il-23 in the body appears to drive chronic inflammatory disease.
journal reference: nature (doi: 10.1038/nature04808)
