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New study helps develop treatments targeting inflammation without affecting gut function

A type of immune cell that contributes to inflammatory bowel disease exists in two forms, 'good' and 'bad'.

A new Crick-led study in Immunity has characterized these distinct populations, which could help scientists to develop treatments targeting inflammation while preserving healthy gut function.

These two populations are akin to worker and soldier ants, playing different roles depending on their context.

The ‘worker ant’ population of immune cells is found naturally in the gut and helps keep the lining of the intestines healthy. The other population is triggered in response to infection by a pathogen. Similar to soldier ants, these immune cells are called in to help fight infection, traveling from lymph nodes – where they are produced – to the gut and other parts of the body to attack the invading pathogens. Although they are necessary to fight infection, these cells can cause excessive inflammation.

By studying the differences between these two cell populations in mice, a multidisciplinary research team has revealed potential ways to target the cells associated with immune-inflammatory diseases, while sparing the ones that help keep the gut healthy.

T helper 17 (Th17) cells have a known role in inflammatory disorders, but also help to keep the gut lining healthy. Previous studies attempting to distinguish between these two functions have studied Th17 cells in isolation in culture dishes, failing to mimic the complex biology of the immune system and microbiome inside the body.

The gut flora-activated Th17 cells kept their function as a protective barrier and did not cause inflammation. By contrast, the pathogen-activated Th17 cells vigorously released pro-inflammatory signals and caused widespread inflammation.

“Th17 cells clearly have many roles in the body – and we need them to fight off infection and keep our intestines healthy,” says Gitta Stockinger, Crick group leader and senior author of the paper. “Any treatment for inflammatory disease would need to dampen the abnormal attack of Th17 cells on healthy tissues, without causing digestive complications or an inability to fight off germs.”

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Posted on: June 28 2019

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