Cross-talk between the complement and the kinin system in vascular permeability.

Area of Science:

• Immunology
• Vascular Biology
• Complement and Kinin Systems

Background:

• The endothelium regulates vascular permeability, interacting with complement and kinin systems.
• These systems, particularly when activated, can induce vascular leakage, implicated in conditions like angioedema (AE).
• Crosstalk between complement and kinin systems is increasingly recognized in pathological processes.

Purpose of the Study:

• To review the roles of complement and kinin systems in vascular leakage.
• To discuss the cross-talk between these systems in the context of angioedema development.
• To explore potential therapeutic targets related to these interactions.

Main Methods:

• Literature review focusing on the interplay between complement and kinin systems in vascular leakage.
• Analysis of evidence implicating bradykinin and its receptors in angioedema pathogenesis.
• Discussion of the roles of B1, B2 receptors, and gC1qR/p33 in angioedema attacks.

Main Results:

• Bradykinin (BK) is identified as a primary mediator of endothelial leakage in AE, acting through B2 receptors.
• While complement system components like C2 were initially suspected, evidence strongly points to BK.
• The potential involvement of B1 receptors and gC1qR/p33 in AE onset and maintenance is highlighted.

Conclusions:

• The interplay between complement and kinin systems significantly contributes to vascular leakage in angioedema.
• Bradykinin, via B2 receptors, is a crucial mediator, but other molecules and receptors warrant further investigation.
• Targeting these receptors presents a promising avenue for novel AE therapies.