It is obvious from the above discussion that, whereas no really clear-cut animal model of IBD has been established, a number of specific insights into the nature of the human illness can be derived from the study of naturally occurring and induced gastrointestinal inflammations occurring in animals. One of the most important emerges from the finding that both immune complex deposition in the gastrointestinal tract as well as stimulation of the mucosal T-cell system results in an ulcerative colitis-like gastrointestinal inflammation. The simplest explanation of the fact that vastly different methods of inducing immune-mediated injury in the gastrointestinal tract can lead to a similar kind of gastrointestinal inflammation is that the inflammatory response in the gastrointestinal tract is rather restricted in its overall pathologic appearance and that the histologic lesions characteristic of ulcerative colitis and Crohn's disease can arise from primary disturbance of the B-cell system, the T-cell system, or both. Another explanation of this fact, however, is that no matter what the initial immunological disorder may be, the mechanism underlying the gastrointestinal inflammation ultimately comes to involve a response to materials in the mucosal environment so that pathologic events are inevitably channeled into an inflammatory pathway that is either ulcerative colitis-like or Crohn's disease-like in its final configuration. This second explanation is buttressed by other findings derived from the study of animal models which, in general, suggest that no matter what the initial result, an immunologic interaction against a constituent of the bowel flora determines the ultimate course of the gastrointestinal inflammation.(ABSTRACT TRUNCATED AT 250 WORDS)