Despite of the extensive spent efforts and money on research on Inflammatory Bowel Diseases (IBD) over the last sixty years, the aetiology of these diseases is still largely unknown. Subsequently no highly effective management has been designed yet.

It was proposed that IBDs were likely to be due to persistent intensified T-cell activation in response to bacterial components. However, the emergent information from the recently reported studies challenge this proposal and evidently prove its impracticality.

The immune system like other biological systems is subject to complex regulatory control. When a normal immune response is initiated by antigenic stimulation, mechanisms must be in place to control the magnitude of that response and to terminate it over time. Down-regulation should contribute to the homeostatic control of all immune responses serving to limit clonal expansion and effector cell activity in response to any antigenic stimulus.

The recent experience suggests that polymorphism of the suppressor genes of the immune responses is significantly contributing to the development of IBD.