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Abstract Number: 547

Anti Ribosomal P  Antibodies Accelerate Lupus Glomerulonephritis and Induce Lupus Nephritis In Naive Mice

Dana Ben-Ami Shor1, Miri Blank2, Sandra Reuter3, Torsten Matthias4, Alexander Volkov5, Iris Barshack6 and Yehuda Shoenfeld7, 1Zabludowicz Center for Autoimmune Diseases, Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, affiliated to Sackler Faculty of Medicine, Tel-Aviv University, Ramat Gan, Israel, 2Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, affiliated to Sackler Faculty of Medicine,Tel Aviv University, Tel-Aviv, Tel-Aviv, Israel, 3AIRA e.V., AESKU.KIPP Institute, Wendelsheim, Germany, 4AESKU.Diagnostics GmbH & Co. KG, Wendelsheim, Germany, 5Institute of Pathology, Sheba Medical Center, affiliated to Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Tel-Aviv, Israel, 6Institute of Pathology, Sheba Medical Center, affiliated to Sackler Faculty of Medicine, Tel-Aviv University,Tel-Aviv, Tel-Aviv, Israel, 7Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Affiliated to Sackler Faculty of Medicine, Tel-Aviv University,Tel-Aviv, Tel-Aviv, Israel

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Auto-immunity, autoantibodies and systemic lupus erythematosus (SLE)

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Session Information

Title: Systemic Lupus Erythematosus - Animal Models

Session Type: Abstract Submissions (ACR)

Background/Purpose: Circulating anti-phosphoribosomal protein antibodies (anti-Ribos.P) were found to be associated with lupus nephritis. We have assessed the direct role of anti-Ribos.P in the development of glomerulonephritis  in-vitro and in animal models. 

Methods: NZBxW/F1 lupus prone mice were immunized with recombinant Ribos.P0 (rRibos.P).  The following lupus parameters were analyzed: autoantibodies screen directed to Ribos.P, dsDNA and Sm by ELISA. Proteinuria was determined by protein-sticks, kidney pathology by H&E staining and  immunoglobulin deposits by immunofluorescence. Anti-Ribos.P deposited in the  glomerular mesangium were eluted from the kidney. Anti-Ribos.P monoclonal Ab was prepared from the rRibos.P immunized NZBxW/F1 mice by hybridoma technology.  . MAPKs expression was analyzed by MAPKs protein-array and confirmed by real-time PCR. To elucidate whether anti-Ribos.P induce glomerulonephritis, naïve C3H mice were immunized with recombinant Ribos.P0 (rRibos.P) and the glomerulonephritis was followed up as described above. 

Results: Our data demonstrate that  rRibos.P0 immunized NZBxW/F1 mice  developed accelerated glomerulonephritis characterized by anti-Ribos.P deposition in the glomerular mesangium . Primary mesangial cells exposed to mouse anti-Ribos.P mAb originated from the immunized lupus mice and to human anti-Ribos.P Abs , induced p38a MAPK expression. Moreover, naïve C3H/Hen mice immunized with rRibos.P0 developed experimental lupus nephritis manifested by circulating autoantibodies directed to Ribos.P, dsDNA, Sm and glomerulonephritis with anti-Ribos.P depositions. In conclusion,   Our data show for the first time that anti-Ribos.P are nephritogenic autoantibodies, as illustrated by in-vitro and in-vivo experiments: a) They accelerate the development of glomerulonephritis in lupus prone mice; b) They induce nephritis in naïve mice. c) Anti-Ribos.P Abs trigger MAPKs expression in primary mesangial cells.

Conclusion: These data contribute a direct mechanistic link between anti-Ribos.P and nephritis in lupus mice.


Disclosure:

D. Ben-Ami Shor,
None;

M. Blank,
None;

S. Reuter,
None;

T. Matthias,
None;

A. Volkov,
None;

I. Barshack,
None;

Y. Shoenfeld,
None.

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