IgE generation and mast cell activation

Franco Pandolfi, Giuliano Giorgio Cerulli, S. K. Kritas, A. Caraffa, P. Antinolfi, A. Saggini, A. Pantalone, G. Neri, M. Rosati, M. Tei, A. Speziali, R. Saggini, G. Cerulli, P. Conti

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

IgE is an important marker for allergy and plays a central role in the induction of allergic diseases through its binding of the high affinity receptor on mast cells. Mast cells can influence B cell survival, proliferation and differentiation into CD138+ cells. Among TH2 cytokines, interleukin (IL)-4 and IL-13 are responsible for class-switching in B cells which resolves in production of allergen-specific IgE antibodies that bind to specific receptor on mast cells. IgE synthesis by B cells is regulated by CD40 ligand, IL-4 and interferon-gamma, therefore inhibition of B cell antigen-specific IgE may prevent the cleavage of CD23 from B cells, having a therapeutic impact which also includes the removal of circulating free IgE, omalizumab, corticosteroids, mast cell stabilizers, leukotriene receptor antagonist, and others. B cell differentiation into IgE-producing cells requires two signals provided by TH2 cells and IL-4, however IL-4, IL-1 and IL-10 as well as several hormones are critical for the development of TH2 cells, while cytokines, such as interferon (IFN)-alpha, IFN-gamma, IL-12 and transforming growth factor (TGF)-beta play a negative role. However, the exact mechanism of this process has not yet been defined.
Original languageEnglish
Pages (from-to)21-25
Number of pages5
JournalEuropean Journal of Inflammation
DOIs
Publication statusPublished - 2014

Keywords

  • IgE

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