The immune system of the gut is controlled by a number of different types of cell. It is kept in balance by communication between these cells through molecules called cytokines. These cytokines can either increase or reduce the immune response, and inflammation can arise when their balance is disturbed. The aim of the current study is to test whether antibodies to cytokines influence the pattern and severity of inflammation in IBD, and the response to treatment.
The cytokine interleukin 10 (IL10) is anti-inflammatory. It adjusts the gut’s immune system in health, and helps turn off the immune response following infection or inflammation. In studies by us and others it has been shown that genetic changes in IL10 play a role in causing IBD in some people. Complete loss of IL-10 function causes severe onset IBD even in babies; while partial loss of IL10 function contributes to adult forms of IBD.
In a major breakthrough we have recently found evidence that in some young children severe IBD is caused by antibodies to IL10. We have explored this further in a group of adolescent and adult patients with IBD recruited in Oxford, and found that a small proportion of them also have antibodies to IL10. We now wish to explore this observation in more detail using samples and data from IBD patients who have been recruited to the IBD BioResource and who are under the care of the gastroenterology teams in Oxford, Cambridge and Newcastle. In existing blood samples we will look for the presence of auto-antibodies to IL-10 (and other cytokines) and evidence of previous triggering viral infection, look at whether the presence of IL10 antibodies makes IBD more severe, and look to see whether the genetic background of patients influences the risk of this happening.
