%0 Journal Article
%T Mechanisms of allergen-specific immunotherapy
%A Hiroyuki Fujita
%A Michael B Soyka
%A M¨¹beccel Akdis
%A Cezmi A Akdis
%J Clinical and Translational Allergy
%D 2012
%I BioMed Central
%R 10.1186/2045-7022-2-2
%X The immune system is a complex interactive network with the capacity of protecting the host from a number of pathogens while keeping a state of tolerance to self and innocuous non-self antigens. Allergy is one of the immune tolerance-related diseases that arises as a direct consequence of a dysregulated immune response. Currently, allergen-specific immunotherapy (allergen-SIT) by the administration of increasing doses of allergen extracts remains the single curative approach to allergic diseases with the potential to modify its course [1,2]. The aim of this review is to discuss the mechanism of allergen-SIT and the current clinical and experimental evidence in the field of immune tolerance induction in allergic diseases.Allergic diseases represent complex innate and adaptive immune responses to environmental antigens leading to inflammatory reactions with a T-helper-2-type cell and allergen-specific IgE predominance [3,4]. CD4+ Na£¿ve T cells differentiate into distinct T cell subsets such as Th1, Th2, Th9, Th17 and Th22 type memory and effector cells depending on the cytokines, other molecules and cells present in the microenvironment [5]. Once a Th2 shift is established, the mechanism of allergic diseases consists of two main phases. In the early phase sensitization and the development of memory cells takes place. The late phase is characterized by inflammation and tissue injury caused by effector cell action. During the sensitization phase, the differentiation and clonal expansion of allergen-specific CD4+ Th2 cells, with the capability of producing IL-4 and IL-13, are essential in the induction of class switching to the ¦Å immunoglobulin heavy chain in B cells and the production of allergen-specific IgE antibodies. Allergen-specific IgE binds to the high affinity receptor Fc¦ÅRI, on the surface of mast cells and basophils as well as to antigen presenting cells (APCs), which in turn allows for an increased uptake of allergens [6]. The engagement of IgE on effector c
%U http://www.ctajournal.com/content/2/1/2