Abstracts (complete list) - Wissenschaft Online

Anjana Singh, Miri Blank, Yehuda Shoenfeld, Harald Illges
Antiphospholipid syndrome patients display reduced titers of
soluble CD21 in their sera irrespective of circulating anti-beta-
2-glycoprotein-I autoantibodies.
B cells have a central role in the development of many autoimmune diseases, relating to
their mechanism of activation, genetics and the successful application of anti-B-cell
therapy. The membrane protein complex CD19/CD21 couples innate immune
recognition by the complement system to the activation of B cells. A soluble form of the
complement receptor CD21 (sCD21) is shed from the lymphocyte surface. sCD21 is able
to bind all known ligands such as CD23, sCD23, Epstein-Barr-Virus and C3d in immune
complexes. The levels of sCD21 in the serum may modulate the immunity. Here, we
show the serum levels of sCD21 in sera of Antiphospholipid syndrome (APS) patients.
APS is an autoimmune disorder in which autoantibodies cause heart attack, stroke and
miscarriage. APS might 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-ß2-GPI autoantibodies. We show that
autoimmune APS patients have significantly reduced amounts of sCD21 in their sera,
irrespective of the presence of anti-ß2-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.