What role does the immune response play in the initiation and pathology of ulcerative colitis?

For anyone who's curious, I found my own answer:

Ulcerative colitis (UC) is an autoimmune disease with a genetic factor that causes those inflicted to develop an immune reaction against their own bowel (Sartor, 2009). It is believed that UC is triggered by some form of stress or disruption in the bowel that initiates an immune response (Sartor, 2009). Those suffering with UC induce a Th2 response, which induces the production of IL-5, IL-6, and IL-10. IL-6 inhibits apoptosis, which skews the proliferation:death ratio causing an extremely strong immune response. Adhesion factors E-selectin and ICAM-1 have a major role in drawing immune cells to the site of infection. It is hypothesized that E-selectin is involved in the early stages of UC, while ICAM-1 is responsible for the persistence of the disease. Patients with UC display a decrease in Treg cells, and an increase in Th17 cells, resulting in an overactive immune response. At the same time, an increase in Il-17a, IL-1beta, IL-6, and TGF-beta was observed in the mucosa of UC patients. These cytokines are proinflammatory, and also increase the production of Th17 cells. The cytokine environment and abundance of proinflammatory molecules helps trigger UC.
The body's flora in the digestive tract also seem to trigger and prolong UC. These bacteria “can stimulate immune responses either by functioning as adjuvants or antigens”. When acting as adjuvants, commensal bacteria activates antigen presenting cells, while as antigens the bacteria stimulates clonal expansion of T cells. Bacterial adjuvants, including peptidoglycan and bacterial flagellin bind to toll like receptors (TLRs) on innate immune cells, which activates NF kappa B (NFKB) which in turn induce the production of pro-inflammatory proteins.
The importance of commensal bacteria to this condition can be illustrated by the fact that in many animal models, UC fails to develop if there is no commensal bacteria present. However, the pairing of bacterial strain and animal species appears to be very specific: mice colitis seems to be paired with E. faecalis and E. coli, while rats tend to be resistant to those two bacteria but susceptible to colitis onset when exposed to Bacteriodes vulgatus. It also appears that different types of bacteria have different effects on UC. For example in mice, E. faecalis-induced UC was slow to progress with onset 10-12 weeks after exposure to the bacteria, while while E. coli had onset 3 weeks after exposure but caused a more moderate inflammation. It is clear that commensal bacteria have an important and specific role in UC.
Activation of macrophages by bacterial PAMPS stimulates the production of many cytokines, including but not limited to IL-1beta, TNF, IL-6, IL-8, adhesion molecules, and other proinflammatory molecules. The activation of NFKB activates MHC class 2 and costimulatory molecules, which then activate Th1 and Th17 cells.
Testing the role of commensal bacteria in human UC could prove to be difficult: different bacteria types cause varying severity of colitis, and different species tend to have different reactions to the same strain of bacteria. Animal models should be used to get an idea of the effects that bacteria have on UC: animals can be brought up in sterile environments and then exposed to the bacteria via a swab that deposits strains of commensal bacteria into the animal's gut lining. Because UC has a genetic component, animal models should be selected accordingly: IL-10-/ mice and HLA-B27 transgenic rats are both good candidates. These trials would determine which bacterial strains play important roles in the disease. However because bacterial and species pairings tend to be very specific in UC, human tests need to be done also. People with UC willing to undergo testing should be categorized based on severity of the disease, and then swabbed. These swabs could then be grown in petri dishes to determine what bacteria is growing in that patient's gut. The results of the swabs could then be compared to the likely bacterial contributors determined by the animal trials. By categorizing the severity of UC of each person, it may be possible to link different strains of bacteria to varying disease severity.

You may also know that Crohn's disease is an autoimmune disease of the gut that has been successfully treated with endoparasites (specifically, pig worms).