In class this past Tuesday, Dr. Cohen mentioned Epstein-Barr virus (EBV) and its role in triggering Burkitt lymphoma. He mentioned briefly how EBV infects B lymphocytes; I thought I would share how our lab uses this phenomenon as part of our research.
I work in a lab dedicated to researching the pathogenesis of the autoimmune disease systemic lupus erythematosus. We are specifically focused on the role of Complement Receptor 2 (CR2), a receptor found primarily on the surface of B cells. This receptor is actually involved in both innate and adaptive immune responses due to the variety of ligands with which it interacts. Among these ligands are gp 350/220, found on EBV. Once EBV has entered the B cell, it acts as an internal mitogen and the infected cell begins to proliferate.
Our lab actually cultivates EBV from a special cell line. We periodically collect supernatant from this cell culture and then use it to “transform” human peripheral blood mononuclear cells into immortalized B cell lines. After infection with EBV, the B cells begin to proliferate and within a week form visible “clumps.” The cells will usually continue to divide as long as I add fresh “cell chow.” Once I have a sufficient number of healthy B cells, I freeze them using a special freezing media. The cells can later be thawed and grown in culture again!
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