Determination of serologic and genetic markers aid in the determination of the clinical course and severity of patients with IBD

In the last decade unprecedented progress has been made in advancing our understanding of the pathophysiology underlying inflammatory bowel disease (IBD). We now know that, at least in part, genetically determined defects in innate, and perhaps adaptive, immunity alter the way our mucosal immune system interacts with our resident bacterial flora.1 This dysregulated interaction leads to the (mal)adaptive immune response that is, in large part, responsible for the chronic inflammatory lesions, characteristic of patients with IBD. The seroreactivity to specific microbial antigens that can be seen in a subgroup of patients with IBD likely represents a surrogate measure of this adaptive immune response. Since reactivity to yeast oligomannan (anti-Saccharomyces cerevisiae antibody; ASCA) was first described in Crohn's disease (CD), the number of CD-specific antigens for which reactivity can be measured has expanded to include the Pseudomonas fluorescens-related protein (I2), Escherichia coli outer membrane-porin (OmpC), and CBir1 flagellin (CBir1).2,–5 In addition, since first described perinuclear antineutrophil cytoplasmic antibodies (pANCA) have emerged as an important marker of the immune response in patients with ulcerative colitis (UC) and patients with a colonic, UC-like CD phenotype.6,–8