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Related Experiment Video

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High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment

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Soluble complement receptor type 1 (CD35) is released from leukocytes by surface cleavage

C Danielsson¹, M Pascual, L French

¹Laboratory of Immunonephrology, Medizinische Klinik B, Department Innere Medizin, Kantonsspital Basel, Switzerland.

European Journal of Immunology

|November 1, 1994

Summary

Soluble complement receptor type 1 (sCR1) in plasma is shed from cell surfaces, primarily polymorphonuclear leukocytes (PMN). This study developed an assay to show sCR1 is an extracellular fragment, not recognized by membrane-bound CR1 assays.

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Area of Science:

Immunology
Complement System Biology

Background:

Soluble complement receptor type 1 (sCR1) in human plasma is thought to originate from cell surface receptor shedding.
Understanding the source and nature of sCR1 is crucial for its role in complement regulation.

Purpose of the Study:

To develop a specific assay for membrane-bound CR1 (mCR1) to differentiate it from soluble CR1 (sCR1).
To investigate the cellular origin and release mechanism of sCR1 in human plasma.

Main Methods:

Developed a novel enzyme-linked immunosorbent assay (ELISA) targeting the intracellular domain of CR1 (mCR1-ELISA).
Tested mCR1-ELISA's specificity using various cell types (erythrocytes, PMN, lymphocytes) and recombinant proteins.
Induced sCR1 release from PMN in vitro using inflammatory stimuli.

Main Results:

The mCR1-ELISA specifically detected membrane-bound CR1 but not plasma sCR1 or recombinant soluble CR1, confirming sCR1 is an extracellular fragment.
Polymorphonuclear leukocytes (PMN) and HL60 cells released a soluble CR1 fragment not detected by mCR1-ELISA.
Inflammatory stimuli (FMLP, TNF-α, LPS) accelerated sCR1 release from PMN, while GM-CSF sustained CR1 expression and release.

Conclusions:

Soluble CR1 is produced by proteolytic cleavage of cell surface CR1.
A significant portion of human plasma sCR1 is released from PMN.
Leukocyte-derived sCR1 may regulate complement activation at inflammatory sites.