Chronic inflammation caused by a malfunction of the immune system is a central medical problem. Following antigen-dependent clonal activation, expansion and affinity maturation, T and B lymphocytes are primary mediators of chronic inflammation and contribute to the pathogenesis of inflammatory diseases such as systemic lupus erythematosus (SLE) and inflammatory bowel disease (IBD), including its two major entities ulcerative colitis (UC) and Crohn's disease (CD). During development and following activation, each T and B lymphocyte is positively or negatively selected on the basis of its individual antigen-receptor, resulting in the elimination or expansion of certain lymphocyte clones. Diversification of the B lymphocyte repertoire is further established through the process of somatic hypermutation, leading to memory cells producing antibodies of higher affinity and greater pathophysiological potential.