Current and Future Treatment of Peanut Allergy Brian P. Vickery, MD, Motohiro Ebisawa, MD, PhD, Wayne G. Shreffler, MD, PhD, Robert A. Wood, MD  The Journal of Allergy and Clinical Immunology: In Practice  Volume 7, Issue 2, Pages 357-365 (February 2019) DOI: 10.1016/j.jaip.2018.11.049 Copyright © 2018 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Figure 1 Mechanisms of food allergy and its treatment. Signals in the local mucosal microenvironment (tissue damage; dysbiosis) promote the release of the epithelial cytokines interleukin (IL)-25, IL-33, and thymic stromal lymphopoetin (TSLP). These conditions influence antigen presentation and favor the development of innate and adaptive immune responses that promote allergic inflammation (bold arrows), ultimately leading to the production of immunoglobulin E (IgE). IgE sensitizes mast cells by binding to its high-affinity receptor and, when cross-linked upon re-exposure to allergen, causes the release of vasoactive mediators that result in allergic symptoms. Commonly used rescue medications partially palliate these symptoms but do not affect the immune response upstream of sensitized mast cells. However, all forms of AIT studied to date are immunomodulatory and appear to affect the functioning of T and B cells. New biologics are under study in food allergy development programs that target the molecules depicted in bold. EPIT, Epicutaneous immunotherapy; IT, immunotherapy. Adapted with permission from Renz H, Allen KJ, Sicherer SH, Sampson HA, Lack G, Beyer K, et al. Food allergy. Nat Rev Dis Primers 2018;4:17098. The Journal of Allergy and Clinical Immunology: In Practice 2019 7, 357-365DOI: (10.1016/j.jaip.2018.11.049) Copyright © 2018 American Academy of Allergy, Asthma & Immunology Terms and Conditions