Infection and cancer trigger immune responses in humans, which associated inflammation can further promote. However, as we are all too aware, the immune system often fails to recognize and eliminate cancer cells. In fact, aspects of the immune response can even be used to a cancer cell's advantage.
On page 11, Glenn Dranoff discusses how cytokines — proteins that regulate the growth, differentiation and activation of immune cells — can promote cancer-cell growth, reduce apoptosis and facilitate metastasis. He discusses promising vaccination techniques that have been designed to recruit granulocytes and macrophages to the tumour and suggests that “combination approaches that both stimulate protective host responses and inhibit immune subversion tactics are likely to prove most efficacious” in eradicating tumours.
Unfortunately, macrophages can also promote tumour progression. Some macrophages can be 'educated' by the tumour microenvironment to facilitate angiogenesis and motility — so argues Jeffrey W. Pollard in an Opinion article on page 71. He suggests that we could target these tumour-associated macrophages using strategies that reduce their recruitment to sites of chronic inflammation. Inhibiting inflammatory cytokines, which would normally attract the macrophages, is one option.
Finally, even if an antitumour host immune response is mounted successfully against cancer cells, it can cause serious side effects, such as paraneoplastic disorders. These autoimmune degenerative diseases are caused — as Matthew Albert and Robert Darnell explain on page 36 — by an immune response against neuronal antigens that are expressed not only in the cancer cells, but also in normal cells in the central nervous system. The authors suggest that therapies that help to coordinate the activation of helper and cytotoxic T cells could limit autoimmune responses.
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In this issue. Nat Rev Cancer 4, 1 (2004). https://doi.org/10.1038/nrc1270
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DOI: https://doi.org/10.1038/nrc1270
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