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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Ann+Rheum+Dis 2016 ; 75 (3): 617-22 Nephropedia Template TP
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Interaction between innate immunity and Ro52-induced antibody causes Sjögren?s syndrome-like disorder in mice #MMPMID25906316
Szczerba BM; Kaplonek P; Wolska N; Podsiadlowska A; Rybakowska PD; Dey P; Rasmussen A; Grundahl K; Hefner KS; Stone DU; Young S; David ML; Radfar L; Scofield RH; Sivils KL; Bagavant H; Deshmukh US
Ann Rheum Dis 2016[Mar]; 75 (3): 617-22 PMID25906316show ga
Objectives: Autoantibodies reactive with Ro52 are often found in sera of Sjögren?s syndrome (SS) patients. This study was undertaken to investigate the role of Ro52-induced immune responses in pathogenesis of SS. Methods: New Zealand Mixed (NZM) 2758 mice were immunized with Ro52 in alum adjuvant. Control mice were immunized either with Maltose binding protein (MBP) or injected with alum alone. Mice were monitored for anti-Ro52 antibody, sialoadenitis and pilocarpine induced salivation. Antibody binding to salivary gland (SG) cells was analyzed in vivo and in vitro by immunofluorescence. Sera from immunized mice were passively transferred into untreated or alum injected NZM2758 mice. Results: By day 30 post-immunization, Ro52 immunized mice generated immunoprecipitating anti-Ro52 antibodies and they had the maximum drop in saliva production. Both Ro52 immunized and control mice showed evidence of mild sialoadenitis. However, only Ro52 immunized mice had antibody deposition in their SG. Passive transfer of Ro52-immune sera induced SG dysfunction in recipient mice, only if the recipients were primed with alum. In vitro, antibodies from Ro52-immune sera were internalized by a SG cell line and this uptake was inhibited by Cytochalasin D treatment. Conclusion: Our data shows for the first time that antibodies induced by Ro52 are capable of inducing SG dysfunction, and that this phenomenon is dependent on the activation of innate immunity. The mouse model described in this study implies that autoantibody deposition in the SG might be an important step in the induction of xerostomia and pathogenesis of SS.