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Related Experiment Video

Updated: Feb 6, 2026

A Cell Free Assay System Estimating the Neutralizing Capacity of GM-CSF Antibody using Recombinant Soluble GM-CSF Receptor

A Cell Free Assay System Estimating the Neutralizing Capacity of GM-CSF Antibody using Recombinant Soluble GM-CSF Receptor

Published on: June 27, 2011

CD21 and FCRL5 form a receptor complex with robust B-cell activating capacity.

Andrea Franco¹, Zachary Kraus¹, Huifang Li¹

¹Office of Biotechnology Products, Center for Drug Evaluation and Research, Food and Drug Administration, Silver Spring, MD, USA.

International Immunology

|August 15, 2018

Summary

Human Fc receptor-like 5 (FCRL5) normally inhibits B-cell receptor (BCR) signaling. However, when co-engaged with CD21, FCRL5 switches to an activating co-receptor, enhancing B-cell responses to immune complexes.

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Last Updated: Feb 6, 2026

A Cell Free Assay System Estimating the Neutralizing Capacity of GM-CSF Antibody using Recombinant Soluble GM-CSF Receptor

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Detection of Neu1 Sialidase Activity in Regulating TOLL-like Receptor Activation

Detection of Neu1 Sialidase Activity in Regulating TOLL-like Receptor Activation

Published on: September 7, 2010

Area of Science:

Immunology
Cell Biology

Background:

B-cell activation is regulated by co-receptors like CD21 and Fc receptor-like 5 (FCRL5).
CD21 amplifies responses to C3 fragments, while FCRL5 was previously thought to inhibit B-cell receptor (BCR) signaling.

Purpose of the Study:

To investigate the interaction and signaling interplay between CD21 and FCRL5 in B cells.
To elucidate the dual signaling capacity of FCRL5 and its regulation by CD21.

Main Methods:

Co-immunoprecipitation to assess physical association between CD21 and FCRL5.
Analysis of signaling molecule recruitment (CD19, PLCγ2, BTK) to FCRL5 upon stimulation.
Calcium flux assays to measure B-cell activation upon co-engagement of BCR, CD21, and FCRL5.
Flow cytometry to identify B-cell subsets co-expressing FCRL5 and CD21.

Main Results:

CD21 and FCRL5 physically associate, enabling simultaneous engagement by immune complexes.
FCRL5 recruits activating signaling molecules (CD19, PLCγ2, BTK) upon engagement, indicating a novel activating function.
FCRL5 inhibits BCR signaling alone via its ITIMs, but co-engagement with CD21 and BCR leads to superior calcium responses.
This activating function is independent of known FCRL5 signaling motifs.
A subset of tonsil B cells co-expresses FCRL5 and CD21.

Conclusions:

FCRL5 possesses dual signaling capacity, acting as an inhibitory co-receptor or an activating co-receptor.
CD21 acts as a molecular switch, converting FCRL5 from an inhibitor to an activator.
Co-expression of FCRL5 and CD21 in specific B-cell populations allows for robust responses to IgG- and C3-fragment-containing immune complexes.