First discovered ten years ago, A20 was largely ignored as an insignificant link in the chain reaction of inflammation. Scientists thought it was only produced by certain types of white blood cells in a few tissues such as the intestines and thymus. Instead they discovered that the molecule was much more widespread than anticipated and that it was a critical regulator of inflammation in multiple tissues. Within three to six weeks after birth, mice without the gene for A20 spontaneously developed severe inflammation and tissue damage in multiple organs. In contrast, normal mice with A20 had no symptoms despite exposure to ten-fold higher doses of these same stimulants.
Inflammation is part of the normal response to an infection or injury.
When it detects an invader such as bacteria or a virus, the immune system mobilizes urgently to repel the assailants. Immune system cells attack the intruders directly while releasing chemical signals to call in additional troops. One of those signals is a substance known as tumor necrosis factor, or TNF . TNF not only initiates a cascade of other chemical messengers but also increases blood-vessel permeability, allowing white blood cells to pass easily out of the capillaries to reach the site of an infection. Once the immune system regains the upper hand, however, it has to scale back this inflammatory response.