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

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Abstract
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.