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Measuring Erythrocyte Complement Receptor 1 Using Flow Cytometry
Published on: May 19, 2020
[Changes of ECR1 genomic density polymorphism, quantitative expression and the activity of ECR1 natural adhesion in
Yuan-li Mao1, Hai-bin Wang, Zhi-qiang Sun
1Center for Clinic Laboratory Medicine, The 302nd Hospital, Beijing 100039, China.
Insights
Patients with chronic hepatitis show significantly reduced levels of complement receptor type 1 (ECR1) on erythrocytes, indicating defective ECR1 expression. This finding highlights the importance of studying ECR1 in chronic liver disease.
Area of Science:
- Immunology
- Hepatology
- Molecular Biology
Context:
- Chronic hepatitis is a significant global health concern.
- Complement receptor type 1 (ECR1) plays a crucial role in immune regulation.
- Erythrocyte-bound ECR1 function is implicated in various inflammatory and infectious diseases.
Purpose:
- To investigate alterations in genomic density polymorphism, quantitative expression, and immune adhesion activity of erythrocyte complement receptor type 1 (ECR1) in patients with chronic hepatitis.
- To compare ECR1 characteristics between chronic hepatitis patients and healthy individuals.
- To assess the correlation between ECR1 expression levels and the severity of liver disease.
Summary:
- Genomic density polymorphism of ECR1 did not differ significantly between patients and healthy controls.
- Quantitative expression of ECR1 on erythrocytes was significantly lower in chronic hepatitis patients compared to healthy individuals.
- Erythrocyte ECR1 levels were further reduced in decompensated cirrhosis compared to compensated cirrhosis, suggesting a link to disease progression.
Impact:
- The study reveals acquired defects in ECR1 expression in chronic hepatitis, potentially impacting immune responses.
- Findings underscore the clinical relevance of monitoring ECR1 levels in chronic hepatitis patients.
- Understanding ECR1 dysregulation may offer insights into novel therapeutic targets for chronic liver diseases.
Objective:
To study the changes of genomic density polymorphism, quantitative expression and the adhesion activity of complement receptor type 1 (ECR1) on erythrocytes in patients with chronic hepatitis.
Methods:
Polymerase chain reaction (PCR) and Hind restriction enzyme digestion, the quantitative assay of ECR1 and the activity of erythrocytes immune adhesion test were applied.
Results:
The spot mutation rate (25.0%-30.3%) of ECR1 density gene in patients with chronic hepatitis was not significantly different from that of healthy individuals (28.0%). The amount of ECR1 in patients with chronic hepatitis, except for the diseases with normal liver function, was significantly lower than that of healthy individuals (t=9.87,P<0.000 1). The quantitative expression of ECR1 in decompensated cirrhosis was obviously lower than that of compensated cirrhosis (t=2.21,P<0.05).
Conclusions:
Defective expression of ECR1 in chronic hepatitis B may be acquired through central and/or peripheral mechanisms. It is very important to study the quantitative expression in the patients with chronic hepatitis.
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