&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