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Depletion of Specific Cell Populations by Complement Depletion
Published on: February 5, 2010
Complement opsonization is required for presentation of immune complexes by resting peripheral blood B cells
S A Boackle1, M A Morris, V M Holers
1Department of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|December 23, 1998
Summary
Complement receptor 2 (CD21) binding of antigen-antibody complexes facilitates antigen presentation by B cells to T cells, independent of B cell activation. This process enhances T cell responses to influenza virus antigens.
Area of Science:
- Immunology
- Cell Biology
Background:
- Complement receptor 2 (CD21, CR2) is a B cell receptor that binds complement degradation products on antigens or immune complexes.
- Its role in antigen presentation by resting B cells, particularly for soluble immune complexes, has been investigated.
Purpose of the Study:
- To investigate the role of CD21 in mediating antigen presentation of soluble immune complexes by resting B cells.
- To understand the mechanism by which CD21 facilitates antigen presentation and T cell activation.
Main Methods:
- Formation of complement-coated immune complexes using influenza virus and immune serum.
- Incubation of complexes with peripheral blood B cells and assessment of binding via CD21 and CR1.
- Pulsing B cells with immune complexes and evaluating T cell clone responses.
- Analysis of B cell activation markers (CD69, CD86) following CD21 ligation.
Main Results:
- Complement-coated immune complexes bound to B cells in a complement-dependent manner, requiring CD21 or CR1.
- B cells pulsed with complement-containing immune complexes elicited responses from influenza-specific T cell clones.
- CD21 ligation alone did not induce B cell activation markers (CD69, CD86).
- Up-regulation of activation markers required T cell factors, indicating antigen presentation independent of B cell activation.
Conclusions:
- CD21-mediated antigen presentation by B cells occurs independently of classical B cell activation pathways.
- Binding of antigens to CD21 allows antigen-nonspecific B cells to participate in activating antigen-specific T cells.
- This mechanism contributes to T cell activation, particularly in response to complement-associated antigens like influenza virus.
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