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Related Experiment Videos

Autoantibodies in scleroderma.

K M Pollard1, G Reimer, E M Tan

  • 1W.M. Keck Autoimmune Disease Center, Scripps Clinic and Research Foundation, La Jolla, California 92037.

Clinical and Experimental Rheumatology
|September 1, 1989
PubMed
Summary
This summary is machine-generated.

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Scleroderma patients exhibit circulating autoantibodies targeting nuclear and nucleolar antigens, including Scl-70 and centromere proteins. These autoantibodies suggest an antigen-driven autoimmune response potentially originating in the nucleolus.

Area of Science:

  • Immunology
  • Rheumatology
  • Cell Biology

Background:

  • Scleroderma is characterized by a wide array of circulating autoantibodies.
  • Key autoantibodies include those targeting Scl-70 (DNA topoisomerase 1) and centromere/kinetochore proteins.
  • Other identified autoantigens are primarily located in the nucleolus, such as RNA polymerase 1, PM-Scl, fibrillarin, and 7-2 ribonucleoprotein.

Purpose of the Study:

  • To define the spectrum of autoantibodies in scleroderma.
  • To investigate the association of specific autoantibodies with clinical subsets.
  • To explore the potential role of nucleolar antigens in scleroderma autoimmunity.

Main Methods:

  • Serological analysis to detect autoantibodies.
  • Correlation of autoantibody profiles with clinical manifestations (e.g., diffuse scleroderma, CREST syndrome).

Related Experiment Videos

  • Immunological assays to identify autoantigens in cellular compartments.

    • Main Results:

    • Antibody to Scl-70 is primarily found in diffuse scleroderma.
    • Antibody to centromere/kinetochore proteins is associated with the CREST subset.
    • Nucleolar autoantibodies (anti-RNA polymerase 1, anti-PM-Scl, anti-fibrillarin, anti-7-2 RNP) are detected in at least 10% of scleroderma patients.

    Conclusions:

    • The autoantibody response in scleroderma appears to be antigen-driven.
    • Autoantigens involved in scleroderma are present in the nucleolus.
    • These findings may offer insights into the initiating mechanisms of scleroderma autoimmunity.