61.   They are present on the apical membranes of gastric parietal cells and, in some species, colon epithelial cells, where they mediate acid secretion.

62.   Intestinal epithelial cells must also maintain homeostasis in the face of varying rates of transepithelial NaCl transport.

63.   This mechanism seems to be the major means of RVI in gall bladder and renal epithelial cells, hepatocytes, and lymphocytes.

64.   The mechanisms of RVI in other intestinal epithelial cells are not known.

65.   Gastrointestinal epithelial cell proliferation is influenced by many hormonal, paracrine, and intraluminal agents.

66.   Gastrointestinal epithelial cells possess a variety of acid-base transport systems.

67.   This evaluation will require selective assay of acid base transport systems on the apical and basolateral membranes of polarised gastrointestinal epithelial cells.

68.   At concentrations found in the rectal lumen, the salicylates used in inflammatory bowel disease impair the binding of IFN to its receptor on colonic epithelial cells.

69.   In the normal gastrointestinal tract, HLA-DR is constitutively expressed on small intestinal villus cells but not in the crypts or on gastric or colonic epithelial cells.

70.   The data presented here suggest that these compounds may act by impairing the binding of IFN to its receptor on the colonic epithelial cell.