IgE-Bearing B-Cells Undergo Apoptosis to Forestall Allergy

Scientists from the CNRS, INSERM, and the Université de Limoges, working in the Laboratoire Contrôle de la Réponse Immune B et Lymphoproliférations (CNRS/Université de Limoges) have demonstrated that the production of type E immunoglobulins (IgE) by B-lymphocytes induces a loss in their mobility and the initiation of cell death mechanisms. These antibodies, present in small quantities, are the most powerful "weapons" in the immune system and can trigger extremely violent immune reactions or immediate allergies (asthma, urticaria, allergic shock) as soon as their levels rise, even slightly. These findings, published online in Cell Reports on February 12, 2015, elucidate how our bodies restrict the production of IgE in order to prevent an allergic reaction. The title of the article is “Self-Restrained B Cells Arise Following Membrane IgE Expression.” Immunity is based on cells, B lymphocytes, which carry or secrete antibacterial or antiviral "weapons," the immunoglobulins (IgG, IgM, IgA, IgE) or antibodies. Although these weapons of immunity offer protection, they can also sometimes turn on us. This is the case for the most effective of antibodies, IgE, where even infinitesimal traces (these IgE are 100,000 times less abundant than other antibodies) can trigger extremely violent allergic reactions. The lymphocytes that produce IgM, IgG or IgA are numerous, easily identifiable, and persistent (as "memory cells"). For hitherto unexplained reasons, the cells that produce IgE are rare and have thus been the subject of very little study. In order to understand the mechanisms controlling IgE, the scientists first of all used genetic engineering to force cells to produce these antibodies in large numbers. They then succeeded in demonstrating two principal control mechanisms.
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