Generation and Characterization of two Monoclonal Self-Associating IgG Rheumatoid Factors from a Rheumatoid Synovium

Authors

  • Edward W. Lu PhD,

    Postdoctoral Research Immunologist, Corresponding author
    1. Department of Medicine, the Department of Pathology, and the Sam and Rose Stein Institute for Research on Aging, University of California, San Diego.
    • Department of Medicine, 0945, University of California, San Diego, La Jolla, CA 92093
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  • Michael Deftos,

    Research Assistant
    1. Department of Medicine, the Department of Pathology, and the Sam and Rose Stein Institute for Research on Aging, University of California, San Diego.
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  • Helen Tighe PhD,

    Postdoctoral Research Immunologist
    1. Department of Medicine, the Department of Pathology, and the Sam and Rose Stein Institute for Research on Aging, University of California, San Diego.
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  • Dennis A. Carson MD,

    Professor
    1. Department of Medicine, the Department of Pathology, and the Sam and Rose Stein Institute for Research on Aging, University of California, San Diego.
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  • Pojen P. Chen PhD

    Associate Professor of Medicine and Pathology in Residence
    1. Department of Medicine, the Department of Pathology, and the Sam and Rose Stein Institute for Research on Aging, University of California, San Diego.
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Abstract

Objective. To study IgG rheumatoid factor (RF) from rheumatoid synovium.

Methods. We fused the K6H6/B5 human—mouse heterohybridoma with unstimulated rheumatoid synovial B cells to generate IgG-RF—secreting hybridomas.

Results. The RFs from 2 such hybridomas bound specifically to the Fc fragment of human IgG and self-associated to form immune complexes. Such immune complexes are a major characteristic of the pathogenic IgG-RFs in rheumatoid synovium.

Conclusion. IgG-RF—secreting hybridomas have been obtained. Analyses may reveal the underlying mechanisms of the induction of IgG-RF.

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