Cross-linking CD21/CD35 or CD19 increases both B7-1 and B7-2 expression on murine splenic B cells

Area of Science:

• Immunology
• Complement System
• B cell Biology

Background:

• The complement cascade and complement C3 receptors on B cells are crucial for linking innate and acquired immunity.
• B7-1 and B7-2 are key co-stimulatory molecules for T cell activation.

Purpose of the Study:

• To investigate the role of complement receptors CD21/CD35 and CD19 in regulating B7-1 and B7-2 expression on B cells.
• To determine how complement receptor ligation impacts B cell antigen presentation and T cell stimulation.

Main Methods:

• Cross-linking of mouse CD21/CD35 or co-cross-linking with surface IgM on splenic B cells.
• Analysis of B7-1 and B7-2 expression using flow cytometry.
• Assessment of allogeneic mixed lymphocyte reaction (MLR) to evaluate T cell stimulation.

Main Results:

• CD21/CD35 ligation rapidly up-regulated both B7-1 and B7-2 expression on resting B cells within 14 hours.
• CD19 cross-linking also increased B7-1 and B7-2 expression.
• CD21/CD35-enhanced T cell stimulation was significantly blocked by anti-B7-2 and partially by anti-B7-1 antibodies.

Conclusions:

• Complement receptor ligation, particularly CD21/CD35 and CD19, enhances B cell antigen presentation through co-stimulatory B7 molecules.
• Rapid B7-1 upregulation by CD21/CD35 and CD19 is a unique finding, suggesting a significant role for complement in immune activation.
• Complement activation via these receptors provides a critical link between innate and adaptive immunity.