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Antiphospholipid syndrome patients display reduced titers of soluble CD21 in their sera irrespective of circulating anti-β2-glycoprotein-I autoantibodies

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Abstract

A soluble form of the complement receptor CD21 (sCD21) is shed from the lymphocyte surface. The sCD21 is able to bind all known ligands such as CD23, sCD23, Epstein–Barr virus and C3d in immune complexes. Here, we show the serum levels of sCD21 in sera the of antiphospholipid syndrome (APS) patients. Antiphospholipid syndrome is an autoimmune disorder in which autoantibodies cause heart attack, stroke and miscarriage. Antiphospholipid syndrome may appear as primary or in association with systemic lupus erythromatosus (SLE) and other autoimmune diseases. Here, we ask whether APS patients have different sCD21 titers compared to healthy persons and whether sCD21 levels correlate with the presence of anti-β2-GPI autoantibodies. We show that autoimmune APS patients have significantly reduced amounts of sCD21 in their sera, irrespective of the presence of anti-β2-GPI autoantibodies. In our APS patients cohort additional SLE, vasculities, DVT (deep vein thrombosis), fetal loss or thrombosis did not correlate to the reduced level of sCD21.

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Acknowledgments

This work was supported by AUTOROME European Community grant no. LSHM-CT-2004-005264 to HI and MB. AS is a Marie Curie Fellow.

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Authors and Affiliations

  1. Department of Natural Sciences, Immunology and Cell Biology, University of Applied Sciences, von-Liebig-Str. 20, 53359, Rheinbach, Germany

    Anjana Singh & Harald Illges

  2. Center for Autoimmune diseases, Department of Medicine “B” and Human Microbiology, Sheba Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

    Miri Blank & Yehuda Shoenfeld

Authors
  1. Anjana Singh
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  2. Miri Blank
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  3. Yehuda Shoenfeld
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  4. Harald Illges
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Correspondence to Harald Illges.

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Singh, A., Blank, M., Shoenfeld, Y. et al. Antiphospholipid syndrome patients display reduced titers of soluble CD21 in their sera irrespective of circulating anti-β2-glycoprotein-I autoantibodies. Rheumatol Int 28, 661–665 (2008). https://doi.org/10.1007/s00296-007-0503-6

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  • DOI: https://doi.org/10.1007/s00296-007-0503-6

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