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Related Experiment Video

Updated: May 5, 2026

Induction of Alloantigen-specific Anergy in Human Peripheral Blood Mononuclear Cells by Alloantigen Stimulation with Co-stimulatory Signal Blockade

Induction of Alloantigen-specific Anergy in Human Peripheral Blood Mononuclear Cells by Alloantigen Stimulation with Co-stimulatory Signal Blockade

Published on: March 14, 2011

Mononuclear cell complement receptor blockade in primary biliary cirrhosis.

M N Al-Aghbar, J Neuberger, R Williams

|January 1, 1985

Summary

Primary biliary cirrhosis patients have fewer C3b receptors on monocytes and lymphocytes due to serum factors blocking these complement receptors. This immune dysfunction may contribute to liver disease progression.

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Last Updated: May 5, 2026

Induction of Alloantigen-specific Anergy in Human Peripheral Blood Mononuclear Cells by Alloantigen Stimulation with Co-stimulatory Signal Blockade

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Published on: March 14, 2011

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Published on: June 24, 2014

Measuring Erythrocyte Complement Receptor 1 Using Flow Cytometry

Measuring Erythrocyte Complement Receptor 1 Using Flow Cytometry

Published on: May 19, 2020

Area of Science:

Immunology
Hepatology
Cell Biology

Background:

Primary biliary cirrhosis (PBC) is a chronic liver disease characterized by autoimmune destruction of bile ducts.
Monocytes and lymphocytes play crucial roles in immune responses and liver disease pathogenesis.
Receptors for complement fragments (C3b) and Fc fragments are important for immune cell function.

Purpose of the Study:

To investigate the expression and function of Fc and C3b receptors on peripheral blood monocytes and lymphocytes in patients with PBC.
To compare receptor expression in PBC with other chronic liver diseases and normal controls.
To identify potential serum factors responsible for altered receptor function in PBC.

Main Methods:

Sheep red blood cells coated with specific antibodies (IgG1 for Fc receptors, IgM and complement for C3b receptors) were used to detect receptor activity.
Mononuclear cells (monocytes and lymphocytes) were isolated from patients with PBC, other chronic liver diseases, and healthy controls.
In vitro experiments involved pre-incubating normal mononuclear cells with serum from PBC patients to assess the effect on receptor function.

Main Results:

Patients with PBC showed significantly reduced numbers of C3b receptors on monocytes compared to normal controls and patients with other chronic liver diseases.
Fc receptor numbers on monocytes did not differ significantly across the studied groups.
Pre-incubation of normal mononuclear cells with PBC patient serum significantly reduced C3b receptor numbers, an effect mediated by serum factors including complement fragments.

Conclusions:

Peripheral blood monocytes and lymphocytes in PBC patients exhibit a specific blockade of C3b receptors.
This blockade appears to be caused by serum factors, potentially including complement fragments, suggesting a role in PBC pathogenesis.
The findings highlight a potential immune dysregulation in PBC involving complement receptor function.