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Updated: Jul 5, 2026

Measuring Erythrocyte Complement Receptor 1 Using Flow Cytometry
Published on: May 19, 2020
[The association of complement with common connective tissue diseases - a review]
1Onaemisfraedideild Landspitala, Hringbraut, 101 Reykjavik. garason@lsh.is
Insights
A defect in complement
Area of Science:
- Immunology
- Rheumatology
Context:
- Complement system plays a crucial role in immune complex clearance.
- Connective tissue diseases like lupus erythematosus are associated with complement abnormalities.
- Previous research suggests a link between complement defects and immune complex disposal.
Purpose:
- To develop a sensitive assay for measuring serum's ability to prevent immune precipitation.
- To investigate complement function in Icelandic patients with connective tissue diseases.
Summary:
- A novel assay revealed a common defect in complement-mediated immune precipitation prevention in patients with systemic lupus erythematosus and systemic sclerosis.
- This defect is distinct from C4A deficiency and strongly correlates with anti-C1q antibodies.
- The findings suggest a potential role for anti-C1q antibodies in the pathogenesis of immune complex diseases.
Impact:
- Provides a new tool for assessing complement function in immune complex diseases.
- Highlights the significance of anti-C1q antibodies in systemic lupus erythematosus and systemic sclerosis.
- Opens avenues for further research into the pathogenesis and potential therapeutic targets for these conditions.
Abstract:
A strong association has been found between complement and common connective tissue diseases, such as systemic lupus erythema and Henoch Schoenlein Purpura. This has led to the notion that the pathogenesis of such diseases may involve a defect in the safe disposal of immune complexes, which is mediated by complement. To bring further light on this subject, a sensitive assay was developed to measure the ability of serum to prevent immune precipitation. This assay was then employed to study various Icelandic patient groups, and a defect in this function of complement was found to be common in patients with systemic lupus erythematosus and systemic sclerosis. Partial deficiency in complement C4A (C4A Q0) can not account for this defect, as it was not observed in patients with diabetes, gluten-sensitive enteropathy or autoimmune thyroiditis, in which C4A Q0 is common. The defect is strongly correlated with anti-C1q antibodies. Further studies are needed to test the possible role of anti-C1q antibodies in the pathogenesis of immune complex disease.
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