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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.

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