Hypersensitivity reactions in the small intestine. 2. Effects of allograft rejection on mucosal architecture and lymphoid cell infiltrate.

Abstract

SUMMARY Small intestinal mucosa contains both thymus dependent and thymus independent lymphoid cells and thus has the capacity to act via humoral and cellular mechanisms as a site of local immunity and local hypersensitivity. Allograft rejection of mouse small intestine is a model of a local cell mediated reaction. The effects of this clearly defined, immunologically mediated damage on villi, crypts, enterocytes, and lymphoid cell infiltrate have been assessed by comparing the morphology of rejecting allografts with that of isografts and normal small intestine of the same age. In rejection there is infiltration of the lamina propria with lymphocytes, hyperplasia of the crypts of Lieberkuhn, and an eventual sloughing off of the mucosa. Usually, but not always, there is villous atrophy and increased numbers of intraepithelial lymphocytes. However, the morphology of individual enterocytes remains normal throughout rejection and neither plasma cells nor polymorphonuclear leucocytes infiltrate the lamina propria before mucosal ulceration. These results show unequivocally that a local T cell mediated immune response causes villous atrophy and crypt hyperplasia in this animal model, and since there is no evidence of local enterocyte cytotoxicity, a lymphokine may be the link between the activated T cell and the effects on mucosal architecture. We suggest that a local CMI reaction may be the cause of villous atrophy, crypt hyperplasia, and malabsorption in many clinical and experimental conditions, including coeliac disease, food allergy, and intestinal infections.

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1

“…Cell-mediated reactions on the intestinal mucosa have been documented in detail during the graft vs. host reaction (23). This hypothesis is supported by the finding in the mouse model of food-sensitive enteropathy, in which migrated lymphocytes in the intestinal mucosa can proliferate in response to stimulation with a specific antigen (29).…”

Different expression of IL-2 receptor α-chain on a lamina propria T cell population and goblet cells in rats orally tolerized or sensitized to ovalbumin (OA) after colonization with an OA-producing Escherichia coli

“…In inflammation and graft rejection newly recruited activated effector T cells are seen in the basal lamina propria crypt region and elevated MHC class II expression [10][11][12][13]. This was also confirmed in the present study and in a parallel study using a similar protocol [14].…”

The biology and pathobiology of the intestinal intraepithelial lymphocyte: A review of the literature

“…In several documents parameters for CMI in the intestinal mucosa have been rendered valid. These parameters include (1) increased proliferation kinetics of epithelial cells in the Lieberkuhn's crypts followed by an infiltration of the villus epithelium with IEL (7,20,24,48) and (2) lymphocytic migration inhibition in mesenteric lymph nodes (36,37,48). (3) Under the condition of enteric parasitic nematode infestations lymphokines (probably IL-3) produced by activated IEL induce the differentiation of mucosal mast cell precursors into mucosal mast cells and a hyperplasia of the mucin-producing goblet cells (7,20).…”