Chronic inflammation helps tumours grow via interferon

Interferons are signalling molecules that activate the immune system during infections and cell damage. Type II interferon (interferon-gamma) has long been known as an activator of immune cells. But what happens when that signal is chronically present rather than temporary? The researchers published their findings in Science and showed that prolonged type II interferon in tumour cells triggers a chain of reactions that ends up protecting the tumour.

From inflammatory signal to tumour growth

The mechanism works in two steps. Chronic type II interferon stimulates tumour cells to produce mitochondrial RNA (transcripts of genetic information from the cell’s energy structures). That mitochondrial RNA in turn activates type I interferon, a different inflammatory signal. Type I interferon then drives the production of prostaglandins: fat-like molecules that regulate inflammation and, at elevated levels, may promote tumour growth.

The finding is relevant to longevity science because chronic low-grade inflammation (also known as inflammaging) is a recognised driver of aging and age-related disease. Cancer is one of those diseases.

Implications for immunotherapy

Many cancer treatments try to activate the immune system, sometimes precisely via interferon signals. This study suggests that the duration and intensity of that signal are critical. Short-term interferon may be protective; chronic interferon can shift toward promoting tumour growth. That distinction is clinically relevant, but requires confirmation in larger studies and in humans.

The study was conducted in mouse models and cell cultures. The findings are preliminary and the precise role of prostaglandins in this process in human tumours has not yet been established.

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