Targeting the extracellular membrane-proximal domain of membrane-bound IgE by passive immunization blocks IgE synthesis in vivo
- Feichtner, S; Infuhr, D; Achatz-Straussberger, G; Schmid, D; Karnowski, A; Lamers, M; Rhyner, C; Crameri, R; Achatz, G;
Publication Year 2008-04-15, Volume 180, Issue #8, Page 5499-5505
- Journal Title
- JOURNAL OF IMMUNOLOGY
- Publication Type
- Journal Article
- The classical allergic reaction starts seconds or minutes after Ag contact and is committed by Abs produced by a special subset of B lymphocytes. These Abs belong to the IgE subclass and are responsible for Type I hyperreactivity reactions. Treatment of allergic diseases with humanized anti-IgE Abs leads primarily to a decrease of serum IgE levels. As a consequence, the number of high-affinity IgE receptors on mast cells and basophils decreases, leading, to a lower excitability of the effector cells. The biological mechanism behind anti-IgE therapy remains partly speculative; however, it is likely that these Abs also interact with membrane IgE (mIgE) on B cells and possibly interfere with IgE production. In the present work, we raised a mouse mAb directed exclusively against the extracellular membrane-proximal domain of mIgE. The interaction between the monoclonal anti-mIgE Ab and mIgE induces receptor-mediated apoptosis in vitro. Passive immunization experiments lead to a block of newly synthesized specific IgEs during a parallel application of recombinant Bet v1a, the major birch pollen allergen. The decrease of allergen-specific serum IgE might be related to tolerance-inducing mechanisms stopping mIgE-displaying B cells in their proliferation and differentiation.
- AMER ASSOC IMMUNOLOGISTS
- CELL ANTIGEN RECEPTOR; LIVED PLASMA-CELLS; MEMORY B-CELLS; CLONAL DELETION; BONE-MARROW; ANTIBODIES; TOLERANCE; EXPRESSION; RESPONSES
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- Refer to copyright notice on published article.
Creation Date: 2008-04-15 12:00:00Last Modified: 0001-01-01 12:00:00