HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Inoue, H. Articles by Saito, I. Search for Related Content PubMed PubMed Citation Articles by Inoue, H. Articles by Saito, I.

Possible Involvement of EBV-Mediated -Fodrin Cleavage for Organ-Specific Autoantigen in Sjogren’s Syndrome¹

Hiroko Inoue^*,, Kazuo Tsubota, Masafumi Ono, Yasuhiro Kizu, Fumio Mizuno, Kenzo Takada^¶, Koichi Yamada^*, Kumiko Yanagi^*, Yoshio Hayashi^* and Ichiro Saito^2,*

^* Department of Pathology, Tokushima University School of Dentistry, Tokushima, Japan; Departments of Ophthalmology and Oral Medicine, Tokyo Dental College, Chiba, Japan; Department of Microbiology, Tokyo Medical University, Tokyo, Japan; and ^¶ Department of Virology, Cancer Institute, Hokkaido University, School of Medicine, Sapporo, Japan

A cleavage product of -fodrin may be an important organ-specific autoantigen in the pathogenesis of Sjogren’s syndrome (SS), but the mechanisms of -fodrin cleavage remain unclear. Since EBV has been implicated in the pathogenesis of SS, we determined whether EBV activation could induce the SS-specific 120-kDa autoantigen -fodrin. ZEBRA mRNA expression, a marker for activation of the lytic cycle of EBV, was found in the salivary gland tissues from SS patients, but not in those from control individuals. ZEBRA-expressing lymphoid cells were also found in the SS glands in double-stained immunohistochemistry. Furthermore, a significant link between production of Abs against 120-kDa -fodrin and reactivated EBV Ag was found in sera from patients with SS, but not in those from control individuals. EBV-activated lymphoid cells showed specific -fodrin cleavage to the expected 120-kDa fragments in vitro. Pretreatment with caspase inhibitors inhibited cleavage of -fodrin. Thus, an increase in apoptotic protease activities induced by EBV reactivation may be involved in the progression of -fodrin proteolysis in the development of SS.

This article has been cited by other articles:

				M. Ramos-Casals and J. Font Primary Sjogren's syndrome: current and emergent aetiopathogenic concepts Rheumatology, November 1, 2005; 44(11): 1354 - 1367. [Full Text] [PDF]

				A. Bredberg, G. Henriksson, A. Larsson, R. Manthorpe, and A. Sallmyr Sjogren's syndrome and the danger model Rheumatology, August 1, 2005; 44(8): 965 - 970. [Full Text] [PDF]