IgE Generation and Mast Cell Activation

• Published in: European journal of inflammation Vol. 12; no. 1; pp. 21 - 25
• Main Authors: Kritas, S.K., Caraffa, A., Antinolfi, P., Saggini, A., Pantalone, A., Neri, G., Rosati, M., Tei, M., Speziali, A., Saggini, R., Pandolfi, F., Cerulli, G., Conti, P.
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.01.2014; SAGE PUBLICATIONS, INC; SAGE Publishing
• Subjects: Cytokines; Histamine; Monoclonal antibodies; B cells; mast cells; inflammation; IgE
• ISSN: 2058-7392; 1721-727X; 2058-7392
• DOI: 10.1177/1721727X1401200103

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.