Dendritic cells and T-cell responses in IBD

In reading several articles on the pathology of Inflammatory Bowel Disease (IBD), it appears that there are a few common understandings and possible avenues for therapeutics for both Crohn’s disease and Ulcerative colitis. Firstly, IBD typically manifests following an abnormal immune response to luminal (gut) flora. While the cause of this reaction has recently been linked to one or more genetic abnormalities, many researchers are focusing more on what occurs in the induced response, and how such a pathway can be halted before damage to tissue occurs. What appears to be common in both CD and UC is the activation of a T-cell mediated inflammatory response that results in the predomination of effector T-cells over regulatory T-cells, escalating the damaging inflammatory process. What also appears to play a part in both diseases is the presence and activation of dendritic cells. The dendritic cells of the gut reside just beneath the epithelial cells, and through the interstices of the intestinal epithelial cells, project long podocytes into the intestinal lumen for sampling of luminal antigens. After processing and presenting this data, either activation or tolerization results. Since it would be difficult to alter this sampling process, perhaps targeting the process following T-cell activation would be more feasible. In both forms of IBD, the expression of TLR-4 (toll-like receptor 4) is increased by dendritic cells following a helper T-cell response. This receptor, however, is distinct in its association with CD14, enabling presentation of lipopolysaccharide, which thereby induces influx of pro-inflammatory cytokines. If the expression of TLR-4 is common and frequent in both CD and UC, could the complex of this receptor with CD14 somehow be prevented? If so, could this lead to perhaps one method for disabling pro-inflammatory cytokine recruitment?