The complement system is a bio-chemical cascade which helps clear pathogens from an organism. It is one part of the larger immune system. The complement system consists of a number of small proteins found in the blood, normally circulating as inactive zymogens. When simulated by one of several triggers, proteases in the system cleave specific proteins to release cytokines and initiate an amplifying cascade of further cleavages. The end result is massive amplification of the response and activation of the cell-killing membrane attack complex.

Over 20 proteins and protein fragments make up the complement system, including serum proteins, serosal proteins, and cell membrane receptors. These proteins are synthesized mainly in the liver, and they account for about 5% of the globulin fraction of blood serum. The bio-chemical pathways activating the complement system consist of: the classical complement pathway, the alternative complement pathway and the mannose-binding lectin pathway. The differences between the three pathways are the steps that occur before the forming of C5 convertase, i.e. three pathways converge at C5. A schematic diagram is shown below.

Inflammation activates the complement system and induces the crosstalk of classical pathway and lectin pathway by CRP and L-ficolin interaction. Deficiencies or mutations in the complement proteins will lead to infectious and immune-related disease. However, how the two pathways balance each other in the systematic level and the pathophysiological mechanism leading to these diseases are so far unknown. Currently, we are in the process of building a computational model for these complement pathways. This work is being done in collaboration with Prof. Ding Jeak Ling's group from Department of Biological Science, National University of Singapore.