Role of ficolin-3 in acute kidney graft rejection: A new diagnostic tool

The complement system has been implicated in a variety of conditions: autoimmune diseases, sepsis, transplantation, ischemia-reperfusion injuries, traumatic brain injury, infections, and bone biology. Complement activation in kidney transplantation may also induce allograft injury and contribute to delayed graft function. Activation of the complement system leads to the formation of molecules with proinflammatory properties. This may result in the killing of microorganisms, or it may lead to attack of altered self-tissue. The complement system may be activated through either of the three ways; that is, classic, alternative, and lectin pathways. The lectin pathway is initiated by binding of the pattern recognition molecules mannose-binding lectin or the three ficolins (ficolins 1, 2, 3) to the surfaces of pathogens or altered self-cells. It appears that a dual role of ficolin 3 may be present; while one being beneficial, the other be unfavorable effect, which does not result in bacterial or cellular clearance, but may lead to uncontrolled complement activation, resulting in adverse effects on the host. Research group demonstrated that decreased serum ficolin-3 was independently correlated with insulin resistance, and low serum ficolin-3 predicted the development of type 2 diabetes mellitus. Contrastingly, several studies showed that ficolin-3 might be one of the initiating factors involved in kidney rejection.