Involvement of Immune Response Vectors in Atherosclerotic Inflammation. Note:
This figure illustrates the roles of various immune response vectors (I1, I2, I3, and I-reg) in the processes of atherosclerotic inflammation. (1) The formation of an atherosclerotic plaque and its transition to an unstable state depends on the balance of pro-inflammatory and specialized pro-resolvent mediators such as IL-10. (2) I2 dominance at the stable plaque stage promotes fibrosis and competitive inhibition of I1. However, I1 has a more pronounced pro-inflammatory potential and is an obvious mechanism of tissue destruction. (3) Cellular elements I-reg actively secrete anti-inflammatory mediators such as IL-10 to stabilize the atherosclerotic plaque. (4) Factors I3, along with I1, can be prominently activated in unstable plaque formation, where they promote tissue destruction. Nevertheless, M2b can actively secrete not only pro-inflammatory mediators but also IL-10, thereby limiting not only I1 but also I3, including Th17 and neutrophils [494].