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. Author manuscript; available in PMC: 2013 Dec 1.
Published in final edited form as: Curr Opin Immunol. 2012 Aug 10;24(6):700–706. doi: 10.1016/j.coi.2012.07.009

Figure 3.

Figure 3

Schematic representation of sequential immune deviation leading to the beneficial effects of ASIT. Before ASIT, the high frequency of allergen-specific CD4+ T cells in allergic individual is dominated by pathogenic TH2 cells. TH2 cytokines inhibit the differentiation and induction of IL-10-secreting TR1 cells and IFN-g secreting TH1 cells. High allergen dose during the course of ASIT induces apoptosis of CD27-allergen-specific TH2 cells which are typically in the final stages of differentiation. In contrast, the less differentiated CD27+ allergen-specific TH1/TR1 cells are more resistant to apoptosis. Hence, the latter becomes increasingly dominant. Stimulation of TH1/TR1 cells leads to IFN-γ and IL-10 production and the induction of allergen specific IgG4 and IgA that can suppress the Type 1 allergic immune response.