IgE Generation and Mast Cell Activation

Autor: S.K. Kritas, A. Caraffa, P. Antinolfi, A. Saggini, A. Pantalone, G. Neri, M. Rosati, M. Tei, A. Speziali, R. Saggini, F. Pandolfi, G. Cerulli, P. Conti
Jazyk: angličtina
Rok vydání: 2014
Předmět:
Zdroj: European Journal of Inflammation, Vol 12 (2014)
Druh dokumentu: article
ISSN: 1721-727X
1721727X
DOI: 10.1177/1721727X1401200103
Popis: 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.
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