While the etiology and mechanism of Inflammatory Bowel Disease (IBD) is not fully understood, immunologic abnormalities play a role in these diseases. Monitoring of disease progression and response to therapeutics is typically invasive and lacking. Increased recruitment of lymphocytes to the gut has been demonstrated in IBD, leading to inflammation and ultimately to gut tissue damage. Lymphocyte circulation is tightly controlled by trafficking receptors (TRs) that act in combination to govern migration to the target organ. Plasmablasts (PBs) are immature circulating B cells that may reflect tissue localized plasma cells. We hypothesize that the PB blood levels and trafficking patterns can inform on the location of tissue damage and the clinical condition of the patients. Using multicolor flow cytometry we examined PB (IgA+/CD38high) and memory B cell (IgA+/CD19+) blood levels, and TRs expressed on these cells. We show that an increase in IgA+ PB blood levels reflect an aggravated clinical state, and a significantly greater amount of these cells in ulcerative colitis patients express colon associated TRs (CCR10+) as opposed to small intestine associated TRs (CCR9+). Additionally, these trafficking patterns are more evident on IgA+ PBs rather than memory B cells. This work in progress suggests that the analyses of the TR phenotype of circulating immature and mature B lymphocytes may provide valuable information for monitoring disease progression via a less invasive process.