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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. Monoclonal antibodies against human ribosomal P proteins penetrate into living cells and cause apoptosis of Jurkat T cells in culture. Sun, K.H., Tang, S.J., Lin, M.L., Wang, Y.S., Sun, G.H., Liu, W.T. Rheumatology (Oxford, England) (2001) [Pubmed]
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