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a Experimental and Clinical Farmacology Unit, DOMERT Department, Centro di Riferimento Oncologico, IRCCS, National Cancer Institute, Aviano (PN), Italy b Service of Digestive Endoscopy-Gastroenterology, General Hospital, Gorizia (GO), Italy c Division of Medical Oncology A, Centro di Riferimento Oncologico, IRCCS, National Cancer Institute, Aviano (PN), Italy d Blood Bank and Department of Clinical Pathology and Immunohaematology, Centro di Riferimento Oncologico, IRCCS, National Cancer Institute, Aviano (PN), Italy e Anatomy, Centro di Riferimento Oncologico, IRCCS, National Cancer Institute, Aviano (PN), Italy f Gastroenterology, Centro di Riferimento Oncologico, IRCCS, National Cancer Institute, Aviano (PN), Italy
Key Words: celiac disease enteropathy-associated T cell lymphoma T cell receptor 2D-DIGE
Address for correspondence: Valli De Re, Ph.D., Division of Experimental Oncology I, Centro di Riferimento Oncologico Via Pedemontana Occidentale 12, 33081 Aviano (PN), Italy. Voice: 39-0434-659672; fax: 39-0434-659659. vdere{at}cro.it
One complication of celiac disease (CD) is refractory CD. These patients frequently show aberrant intraepithelial T cell clones and an increasing risk of evolution into enteropathy-associated T cell lymphoma (EATL). There is debate in the literature whether these cases are actually a smoldering lymphoma from the outset. The mechanism inducing T cell proliferation and prognosis remains unknown. Recently, alemtuzumab has been proposed as a promising new approach to treat these patients. Only few single cases have been tested presently, nevertheless, in all of them a clinical improvement has been observed, while intraepithelial lymphocytes (IELs) effectively targeted by alemtuzumab are still a debated issue. Using 2D-DIGE, we found hyperexpressed proteins specifically associated with aberrant T cell in a patient with CD by comparing the protein expression with that of patients with CD and polyclonal T cell or with that of control subjects (patients with polyclonal T cell and no CD). Proteins with a higher expression in duodenal biopsy of the patient with aberrant T cell were identified as IgM, apolipoprotein C-III, and Charcot–Leyden crystal proteins. These preliminary data allow hypothesizing different clinical effects of alemtuzumab in patients with CD, since besides the probable effect of alemtuzumab on T cell, it could effect inflammatory-associated CD52+ IgM+B cell and eosinophils cells, known to produce IgM and Charcot–Leyden crystal proteins, which we demonstrated to be altered in this patient. Results also emphasize the possible association of apolipoprotein with aberrant T cell proliferation.
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