MADRID, Spain, June 13, 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 reported that epratuzumab, the Company's humanized anti-CD22 antibody, mediates the reduction of select proteins on the surface of B cells via a process known as trogocytosis, and that such reduction could modulate B-cell activities.Results from this study were presented by Edmund A. Rossi, Ph.D., Executive Director, Recombinant Technology. Epratuzumab is currently in two UCB-conducted Phase III pivotal trials for the treatment of patients with systemic lupus erythematosus (SLE). UCB holds the worldwide development rights for epratuzumab in autoimmune diseases, while the Company retains all rights in oncology. In earlier clinical studies in SLE and in non-Hodgkin lymphoma (NHL), epratuzumab has been shown to deplete about 30-40% of circulating B cells in patients. However, the mechanism of action of epratuzumab, especially its involvement in regulating B-cell antigen receptor (BCR) signaling, has yet to be fully elucidated. In this preclinical study, treatment of peripheral blood mononuclear cells (PBMCs) with epratuzumab significantly reduced the levels of select B-cell surface proteins, including CD22, CD19, CD21 and CD79b. Corroboratively, SLE patients on epratuzumab therapy also showed significantly lower levels of CD22, CD19 and CD21, compared to treatment-naïve patients. Although internalization of CD22 upon epratuzumab binding is known and expected, reduction of the other BCR proteins presents a new finding. The reduction of CD19 is of particular interest since elevated levels of this protein on the surface of B cells have been implicated in SLE. Another key finding from this study is the formation of immunological synapses between B cells and effector cells, such as monocytes, natural killer cells and granulocytes, induced by epratuzumab. By binding to B cells and effector cells simultaneously, epratuzumab serves as a conduit for the transfer of the BCR-associated receptors, lowering their presence on B cells.