Allergy season kills…immune cells, that is. New work from the CNRS, INSERM, and Université de Limoges in France identified that “Self-Restrained B Cells Arise Following Membrane IgE Expression” as a means of staving off severe allergy attacks due to antigens that enter the body — a particularly important cascade especially among asthmatics.
IgE is an immunoglobulin — a class of proteins that also includes IgG, IgB, IgM, and IgA — that contributes to immune function and can trigger severe allergic reactions even in low amounts. B cells are the producers of immunoglobulins, which are abundant in the body, but B cells that produce IgE are far less common. Due to their rarity in the body, these B cells are less commonly studied. To understand these cells and the mechanisms behind allergy attacks, the researchers studied genetically engineered cells for altered behavior due to overproduction of IgE.
When IgE is bound to the membrane of cells, it is known as mIgE. B cells decorated with mIgE lose their ability to move after rounding up and losing the membrane protusions that enable migration. While in this immobile state, the B cells undergo apoptosis and die, eliminating the body of IgE carriers.
Writing in Cell Reports, lead author Dr. Brice Laffleur stated, “We show[ed] that, independent of stimulation, mIgE expression per se alters the B cell phenotype in multiple regards, with notably a short lifespan.”
When an antigen enters the body, B cells expressing IgE live just long enough to battle the offending parasite, toxin, or poison that triggered IgE production. However, nothing in nature is perfect, and IgE can be expressed without any antigen encounter. The cell arrest and apoptosis mechanisms studied by Dr. Laffleur and colleagues are the body’s way of protecting itself from extreme allergic reactions. Since IgE is a strong trigger for allergic reactions, it must be tightly controlled. “This phenotype directly imposed by mIgE expression prior to any antigen encounter may explain the short lifespan and in vivo rarity of mIgE+ cells,” wrote Dr. Laffleur.
The authors believe an in-depth analysis of the constraints on IgE expression and B cell survival will lead to a greater understanding of IgE-mediated immune responses. A deeper understanding may result in new therapeutic targets to prevent allergic responses or to reduce pathological B cells in the case of lymphoma.
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