MORRIS PLAINS, N.J., Oct. 25, 2013 (GLOBE NEWSWIRE) -- Immunomedics, Inc. (Nasdaq:IMMU), a biopharmaceutical company primarily focused on the development of monoclonal antibody-based products for the targeted treatment of cancer, autoimmune and other serious diseases, today announced that an article published yesterday in Blood described a mechanism by which epratuzumab affects B cells. Epratuzumab is a humanized anti-CD22 antibody currently in Phase III trials conducted by the Company's corporate partner, UCB (Euronext Brussels:UCB), as a therapeutic for patients with systemic lupus erythematosus (lupus). The article was authored by several scientists of the Company, as well as a clinical collaborator, Dr. Daniel J. Wallace of Cedars-Sinai Medical Center of UCLA in Los Angeles, CA. The article was featured on the cover of this issue of Blood with a fluorescence microscopy image, showing how epratuzumab can translocate certain surface proteins on B cells to other blood cells, a process called trogocytosis. Accompanying the article was an invited commentary by Dr. Ronald P. Taylor of the University of Virginia School of Medicine, who is a pioneer on studies of trogocytosis involving anti-B-cell antibodies, such as rituximab. In the article by Rossi and colleagues of Immunomedics, it was demonstrated that epratuzumab can induce trogocytosis of CD22, CD21, CD19, and several other B-cell surface molecules from lymphocytes to other blood cells, such as monocytes, natural killer cells, and granulocytes. Epratuzumab is distinct from other B-cell antibodies, such as rituximab, because it does not drastically deplete B cells, but instead compromises B-cell autoimmune activity. The Immunomedics scientists postulated that removal of CD22, CD19, CD21 and other proteins from the surface of B cells reduces the autoimmune activity of these cells. In fact, B cells obtained from lupus patients who were treated with epratuzumab showed reduced CD22, CD19 and CD21. The authors suggest that this modulation of B cells via trogocytosis could be the major mechanism of epratuzumab in patients with lupus.