Infl ammatory bowel disease: cause and immunobiology

A large part of this article talked about several primary events seen in patients with inflammatory bowel disease. First, people with IBS tend to have leaky epithelial barriers(increased permeability) preceding the onset of disease. Furthermore, healthy individuals that are first-degree relatives of patients with IBD also show permeability defects. I am curious as to why this does not lead to the disease in these people. Of course, there are other factors but this is a highly genetic disease. Does anybody have insight into this??
Other primary events include:
*disturbed immune mechanisms-different TLR expression, upregulation of NOD2 in epithelial cells, which may compromise the ability to eliminate pathogenic microbes, leading to inflammation.
*disturbed antigen recognition and processing- animals studies show incorrect recognition of commensal bacteria and induction of a proinflammatory response normally caused in response to pathogens. Also, patients show an increase in active dendritic cells that prolong their survival and maintain inflammation, and a decrease in immature dendritic cells. This may contribute to the repeated activation of memory t-cells or failure to delete them.
*atypical antigen presenting cells become potent effector-T-cells
*absense of t-cell apoptosis
*effecor T-cells predominate over regulatory T-cells
***STRESS- increased SNS activity is shown to cause increased colonic paracellular permaeability. I found this to be the most interesting!! The article talks about how the biggest therapeutic challenge is to develop an approach to prevention of the initation of the inflammatory cascade before tissue injury occurs. One thing that we have control over is stress! Maybe if these genetically predisposed people chill out, it will make a difference in there future health status! Although I doubt that this alone will make the difference, it is an important factor in this disease, as well as health in general.