| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
From the Istituto di Scienze dell’Alimentazione,* Consiglio Nazionale delle Ricerche, Avellino, Italy; the Department of Pediatrics and European Laboratory for the Investigation of Food-Induced Diseases, University Federico II, Naples, Italy; Gastroenterologia ed Endoscopia Digestiva,¶ Azienda Ospedaliera "San Giuseppe Moscati," Avellino, Italy; Dipartimento di Pediatria,|| Universita’ di Firenze, Florence, Italy; the Department of Internal Medicine,** University Tor Vergata of Rome, Rome, Italy; the Division of Infection, Inflammation, and Repair, University of Southampton, School of Medicine, Southampton General Hospital, Southampton, United Kingdom; and the Department of Paediatric and Adult Gastroenterology, St. Bartholomews and the Royal London School of Medicine and Dentistry, London, United Kingdom
The biological effects of interferon (IFN)-
rely mainly on the activity of the transcription factor signal transducer and activator of transcription (STAT) 1 and the intracellular levels of suppressor of cytokine signaling (SOCS)-1, a negative regulator that controls the amplitude and duration of STAT-1 activation. IFN- is a key mediator of the immunopathology in celiac disease (CD, gluten-sensitive enteropathy). Thus we have investigated STAT-1 signaling and SOCS-1 expression in this condition. As expected, high local concentrations of IFN- were invariably seen in duodenal biopsies from CD patients in comparison to controls. On the basis of immunohistochemistry, STAT-1 phosphorylation, nuclear localization, and DNA-binding activity, STAT-1 activation was consistently more pronounced in CD compared with controls. Despite samples from CD patients containing abundant SOCS-1 mRNA, SOCS-1 protein was expressed at the same level in CD patients and controls. In explant cultures of CD biopsies, gliadin induced the activation of STAT-1 but not SOCS-1. Furthermore, inhibition of STAT-1 prevented the gliadin-mediated induction of ICAM-1 and B7-2. These data suggest that persistent STAT-1 activation can contribute to maintaining and expanding the local inflammatory response in CD.
This article has been cited by other articles:
 |
|
 |
|
  M. L. Slattery and F.A. Fitzpatrick Convergence of Hormones, Inflammation, and Energy-Related Factors: A Novel Pathway of Cancer Etiology Cancer Prevention Research, November 1, 2009; 2(11): 922 - 930. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Martinez-Lostao, J. Ordi-Ros, E. Balada, A. Segarra-Medrano, J. Majo-Masferrer, M. Labrador-Horrillo, and M. Vilardell-Tarres Activation of the signal transducer and activator of transcription-1 in diffuse proliferative lupus nephritis Lupus, July 1, 2007; 16(7): 483 - 488. [Abstract] [PDF]
|
|
|
|
 |
|
 G. Terrazzano, M. Sica, C. Gianfrani, G. Mazzarella, F. Maurano, B. De Giulio, S. de Saint-Mezard, D. Zanzi, L. Maiuri, M. Londei, et al. Gliadin Regulates the NK-Dendritic Cell Cross-Talk by HLA-E Surface Stabilization J. Immunol., July 1, 2007; 179(1): 372 - 381. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I Monteleone, G Monteleone, G Del Vecchio Blanco, P Vavassori, S Cucchiara, T T MacDonald, and F Pallone Regulation of the T helper cell type 1 transcription factor T-bet in coeliac disease mucosa Gut, August 1, 2004; 53(8): 1090 - 1095. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
