Prior observations over the last 40 years, particularly in humans, have clearly demonstrated that IgM-ALA levels increase with various infections (viral and parasitic), autoimmune diseases (SLE), and other inflammatory states (sarcoidosis and end stage renal disease), and IgM-ALA levels normalize with control of infection or the inflammatory state [reviewed in Ref. This evidence concerns the gene CD40LG and systemic lupus erythematosus.