Cellular immune mechanisms in the pathogenesis of Crohn's disease

Abstract

Crohn's disease is a chronic relapsing inflammatory disease of the intestine of unknown cause. It has been suggested that the disease may result from an abnormality of the immunological functions of the gut. Recent advances in the study of the gastrointestinal immune system show that T cells in the intestinal mucosa are more activated, contain a higher proportion of T4 cells having the phenotypic and functional characteristics of helper-inducer cells, have greater capacity for IL-2 production, and have altered responsiveness to antigen stimulation. In the intestinal mucosa in Crohn's disease the predominance of T cells with helper-inducer function is maintained, and there is no evidence of augmented suppressor activity. Although natural killer cells are infrequent in the intestinal mucosa in Crohn's disease, lymphokine activated killer cell precursors and cytolytic T cell precursors are present and it is possible that these cells also play an important role in the disease. The failure to identify specific infections or environmental etiologies in Crohn's disease is consistent with the hypothesis that the disease is due to an inappropriate immunological hyper-responsiveness to ubiquitous components of the alimentary tract.