The lectin pathway of complement activation is a part of the innate immune system, and serves to eliminate pathogens from the circulation and prevent accumulation of debris and dead cells. Disturbances in these functions lead to infection susceptibility and the development of autoimmunity by incompletely understood mechanisms. In this project we will use a combination of genetic and translational approaches to define the mechanism by which the complement system contributes to the development of systemic lupus erythematosus (SLE), a severe autoimmune disorder with limited treatment options. We have developed novel methods to measure complement in biological samples and have used these methods to profile lectin pathway activity in plasma samples from SLE patients. In order to gain insight into genetic regulation of the lectin pathway, genotyping data will be combined with our proteomic data set to a perform pQTL analysis for lectin pathway activity in SLE patients and healthy controls. For this purpose, resources at the SNIC SENS cluster environment is requested. An application for bioinformatical support from NBIS has already been granted. If successfully completed, the project is expected to yield novel insight into how genetically determined immune function influences propensity for autoimmune diseases.