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Rheumatology 2001; 40: 750-756
© 2001 British Society for Rheumatology


Original Papers

Monoclonal antibodies against human ribosomal P proteins penetrate into living cells and cause apoptosis of Jurkat T cells in culture

K.-H. Sun, S.-J. Tang1, M.-L. Lin, Y.-S. Wang, G.-H. Sun2 and W.-T. Liu

Faculty of Medical Technology and Institute of Biotechnology in Medicine, National Yang-Ming University,
1 Institute of Marine Biotechnology, National Taiwan Ocean University and
2 Division of Urology, Department of Surgery, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan

Objective. This study was designed to determine the role of autoantibodies to the ribosomal P protein (anti-P Abs) in the pathogenesis of systemic lupus erythematosus (SLE) using monoclonal anti-P antibodies (anti-P mAbs).

Methods. Anti-P mAbs were prepared by a standard hybridoma procedure using recombinant human P1 and P2 proteins as immunogens. We studied the reactivities of these mAbs to P proteins, their binding and penetration capabilities in different cell lines and their apoptotic effects on Jurkat T cells.

Results. In addition to recognizing human P0, P1 and P2 proteins, the anti-P mAb 9B6-4 bound to 20–40% and penetrated 50–90% of astrocytes, Jurkat T cells and lung cancer cells via the P0 surface protein. Treatment with the mAb 9B6-4 also caused increases in the percentages of Jurkat T cells in the sub-G1 phase of the cell cycle (14.8%) and undergoing apoptosis (21.3%).

Conclusion. Anti-P autoantibodies may play a role in the pathogenesis of lymphopenia or lymphocyte dysfunction in SLE.

KEY WORDS: Anti-P autoantibody, T lymphocytes, Apoptosis.

Correspondence to: K.-H. Sun, Faculty of Medical Technology, National Yang-Ming University, 155 Section 2, Lie-Nong Street, Taipei, Taiwan 112.


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