RT Journal Article
SR Electronic
T1 Role of interferon α in promoting T helper cell type 1 responses in the small intestine in coeliac disease
JF Gut
JO Gut
FD BMJ Publishing Group Ltd and British Society of Gastroenterology
SP 425
OP 429
DO 10.1136/gut.48.3.425
VO 48
IS 3
A1 G Monteleone
A1 S L F Pender
A1 E Alstead
A1 A C Hauer
A1 P Lionetti
A1 T T MacDonald
YR 2001
UL http://gut.bmj.com/content/48/3/425.abstract
AB Coeliac disease (CD) is caused by a CD4 T helper cell type 1 (Th1) response in the small intestinal mucosa to dietary gluten. As the major Th1 inducing cytokine, interleukin 12, is undetectable in CD gut mucosa, the mechanism by which Th1 effector cells are generated remains unknown. Interferon (IFN) α, a cytokine capable of promoting IFN-γ synthesis, has been implicated in the development of Th1 mediated immune diseases. Here we report a case of CD-like enteropathy in a patient receiving IFN-α for chronic myeloid leukaemia. Morphological assessment of duodenal biopsies taken from the patient showed total villous atrophy, crypt cell hyperplasia, and a high number of CD3+ intraepithelial lymphocytes. Both antigliadin antibodies and antiendomysial antibodies were positive. RNA analysis revealed pronounced expression of IFN-γ. Withdrawal of gluten from the diet resulted in a patchy improvement in intestinal morphology, normalisation of laboratory parameters, and resolution of clinical symptoms. By western blot analysis, IFN-α protein was seen in the duodenal mucosa from untreated CD patients but not in controls. This was associated with marked expression of IFN-γ protein in CD mucosa. Collectively, these results suggest a role for IFN-α in promoting Th1 responses to gluten.CDcoeliac diseaseEMAantiendomysial antibodiesAGAantigliadin antibodiesTh1,T helper cell type 1IFN, interferonILinterleukinIELintraepithelial lymphocyteAPCantigen presenting cell