Our immune system should get rid of any strange body in our organism. Yet, tumors manage to somehow go undetected by the immune system and this is why it does not take action.

Normally, the immune cells form an inflamed area surrounding a dangerous pathogen or injury which signals to the whole immune system the issues. But in the case of tumors, certain cell mechanisms turn off the inflammation, so that the tumor is not attacked and destroyed.

A team at the King's College London, in a recently published research in the Proceedings of the National Academy of Sciences found that regulatory T cells are crucial in triggering the activity of macrophage cells involved in inflammation formation and could be 'fooled' by tumor cells.

Regulatory T cells tune the immune system to impede it over-reacting to every external stimulus (causing allergies) and only mark real harmful germs or injuries. This is done by making macrophages to lower the inflammatory reaction that is automatically triggered by any foreign body, including harmless ones, like pollen or dust.

"A relatively harmless stimulus, such as a small cut, will automatically be treated by the body as something dangerous and will cause macrophages to promote inflammation. We discovered that it is then the regulatory T cells' responsibility to make the macrophages promote anti-inflammation to counteract the initial response, as it is not a real danger. This helps keep the immune system stable and prevents the body over-reacting to everything in its environment." said lead researcher Dr Leonie Taams.

"However problems can occur with tumors, where many regulatory T cells promoting a strong anti-inflammatory response are present. Neutralizing an inflammatory response in this scenario can cause the tumor to fall under the radar of the body's immune system and 'trick' it into believing that there is no problem. We hope to be able to use this new knowledge about the relationship between regulatory T cells and macrophages to find more effective treatments for tumors. Interestingly, we also hope to use the same knowledge to achieve the opposite result and block chronic inflammation such as that which occurs in rheumatoid arthritis." added Taams.