摘要:

&NA;Intraepithelial lymphocytes interspersed between intestinal epithelial cells form a large population of T cells, mainly CD8+, close to the intestinal lumen. Together with lamina propria T cells and plasma cells, they represent the effector limb of the gut‐associated lymphoid system. Recent data highlighting their original properties and their interactions with epithelial cells are reviewed; their contributions to immune defenses and gastrointestinal diseases in humans are discussed.Current Opinion in Gastroenterology 1993,9:953‐961

ISSN:0267-1379    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

&NA;The appropriate recruitment of leukocytes to sites of immune challenge is a fundamental requirement for effective immune defense. Leukocyte trafficking is controlled, to a large extent, by the regulated expression of a variety of cell‐surface adhesion receptors. This review provides an introduction to three families of adhesion glycoproteins: the integrins, the immunoglobulin‐like adhesion receptors, and the selectins. The roles played by these different adhesion molecules in regulating leukocyte‐endothelial cell interactions during the process of neutrophil extravasation is described. The recently characterized &bgr;7integrin adhesion receptors appear to play an important role in directing lymphocyte homing to the gastrointestinal tract. The importance of cell adhesion molecules in gut immune function is not confined to leukocyte‐endothelial adhesion, as shown by a series of recent studies describing adhesion molecule‐mediated interactions between leukocytes and intestinal epithelial cell lines. Other studies highlight the importance of leukocyte adhesion in a variety of gastrointestinal inflammatory states including inflammatory bowel disease, nonsteroidal anti‐inflammatory drug‐induced gastritis, and intestinal ischemia reperfusion injury. The potential for developing new therapeutic agents has provided a major impetus to adhesion molecule research. It is now apparent that many anti‐inflammatory drugs, including such familiar agents as corticosteroids and non‐steroidal anti‐inflammatory drugs, modulate adhesion molecule interactions, and thereby affect the regulation of leukocyte trafficking in intestinal inflammation.Current Opinion in Gastroenterology 1993,9:962‐970

ISSN:0267-1379    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

&NA;There is a growing body of experimental and clinical evidence to suggest that reactive oxygen metabolites (eg, superoxide, hydrogen peroxide, hydroxyl radical, and halogenated oxidants) may play an important role in the pathogenesis of inflammatory bowel disease (eg, Crohn's disease and ulcerative colitis). Recent studies have demonstrated enhanced production of reactive oxygen species in the chronically inflamed colon. The most likely sources of these oxidants are the phagocytic leukocytes (eg, neutrophils, monocytes, and macrophages), which are known to accumulate within the colonic interstitium during times of active inflammation. Many of these leukocyte‐derived oxidants have been shown to mediate cytotoxicity, degrade the extracellular matrix, enhance electrolyte (and water) secretion, alter smooth muscle function, and promote mutagenesis. In addition, the anti‐inflammatory effects of 5‐aminosalicylic acid, a drug with potent antioxidant activity suggests that oxidants and free radicals may be important mediators of the pathophysiology observed in inflammatory bowel disease. Although there is a large volume of circumstantial evidence that implicates oxy radicals in chronic gut inflammation, there is a relative paucity of published reports that have attempted to directly assess the role of free radicals in models of chronic gut inflammationin vivo.This scarcity of information appears to be due to the lack of long‐lived antioxidants with well‐characterized mechanisms of action and specific inhibitors of phagocyte‐associated reactive oxygen generators. The development of new generation, long‐lived antioxidants and specific inhibitors should prove useful in defining a role for reactive oxygen metabolites in inflammatory bowel disease.Current Opinion in Gastroenterology 1993,9:971‐980

ISSN:0267-1379    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

&NA;Results from a recent clinical trial have suggested that the feeding of autoantigenic proteins may be an effective therapy for autoimmune diseases (Weineret al., Science1993, 259:1321‐1326). This treatment, called oral tolerance therapy, proposes to inhibit aberrant immune responses by producing immune “acceptance” or tolerance to target tissue proteins. Because of the innovative nature of this approach, interest has been focused on the regulatory mechanisms that produce the state of oral tolerance. In this review, we address the models of oral tolerance and suggest that this state may involve unique regulatory mechanisms based on the amount of fed protein antigen.Current Opinion in Gastroenterology 1993,9:981‐985

ISSN:0267-1379    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

&NA;Nematode parasites of the gastrointestinal tract occupy different niches on or within the mucosa. The epithelial and mucosal changes have many features that are characteristic of allergic inflammation, including altered epithelial secretion, recruitment of eosinophils, basophils, and mast cells, and production of immunoglobulin E. The role of T‐cell subsets in the induction of these changes is the main focus of this review.Current Opinion in Gastroenterology 1993,9:986‐993

ISSN:0267-1379    

出版商:OVID    

年代:1993

数据来源: OVID

摘要:

&NA;This review highlights recent publications on the subject of gluten sensitivity. The termgluten sensitivityshould supersedeceliac diseasebecause it embraces all individuals of appropriate genetic background whose T cells are sensitized to gluten protein, including all dermatitis herpetiformis cases with immunoglobulin A+skin biopsy results, symptomatic celiac disease patients, and the larger majority with latent (or subclinical) disease. Such individuals are predisposed to intestinal mucosal damage by a remarkably tight association (> 95%) with the DQw2 specificity. A spectrum of mucosal lesions (besides the “flat” lesion) occurs with gluten sensitivity; the milder lesions have yet to be recognized by many physicians and pathologists as caused by gluten in particular and to presumptive T‐cell activity in general. That these are all T‐cell‐mediated lesions is suggested by their similarity to defined immunologic models of enteropathy that have been pursued in experimental animals. The response of rectal mucosa is best explained by the recruitment of sensitized T cells to gluten deposition. Although &ggr;&dgr; cells have excited much interest throughout the immunologic community of late, their role in gluten‐induced mucosal pathology is far from clear. It should also be noted that the tempo of their mucosal appearance and disappearance is much slower than that of CD8 &agr;&bgr; lymphocytes. Antibodies to &agr;‐gliadin remain useful for predicting, and screening for, gluten sensitivity. There is clearly little doubt that gluten sensitivity is an immunologically determined disease and work reviewed herein considerably strengthens that view. Nevertheless, it is hoped that future work with cloned T cells will provide the final, but necessary, piece of evidence that will confirm the view that gluten sensitivity is primarily an immunologically driven condition.Current Opinion in Gastroenterology 1993,9:994‐1000

ISSN:0267-1379    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0267-1379    

出版商:OVID    

年代:1993

数据来源: OVID

ISSN:0267-1379    

出版商:OVID    

年代:1993

数据来源: OVID