Nature of regulatory T cells in the context of allergic disease

Abstract

: Allergen-specific immunotherapy (SIT) is the cornerstone of the management of allergic diseases, which targets modification of the immunologic response, along with environmental allergen avoidance and pharmacotherapy. SIT is associated with improved tolerance to allergen challenge, with a decrease in immediate-phase and late-phase allergic inflammation. SIT has the potential to prevent development of new sensitizations and progression of allergic rhinitis to asthma. It has a role in cellular and humoral responses in a modified pattern. The ratio of T helper (Th)1 cytokines to Th2 cytokines is increased following SIT, and functional regulatory T cells are induced. Interleukin-10 production by monocytes, macrophages, and B and T cells is increased, as well as expression of transforming growth factor beta. SIT is associated with increases in allergen-specific antibodies in IgA, IgG1, and IgG4 isotypes. These blocking-type immunoglobulins, particularly IgG4, may compete with IgE binding to allergen, decreasing the allergen presentation with the high- and low-affinity receptors for IgE (FcepsilonRI and FcepsilonRII, respectively). Additionally, SIT reduces the number of mast cells and eosinophils in the target tissues and release of mediators from these cells.

Figure 1

Allergen-specific immunotherapy (SIT) is associated with improved tolerance to allergen challenge, with a decrease in immediate-phase and late-phase allergic inflammation. SIT also reduces the number of effector cells and release of their mediators in the target tissues. It has a role in cellular and humoral responses. T helper (Th)2 cytokines are decreased, and functional regulatory T cells (Tregs) are induced. Interleukin (IL)-10 production by monocytes, macrophages, B cells, and T cells is increased, as well as expression of transforming growth factor β (TGF-β). SIT is associated with increases in allergen-specific antibodies in IgA, IgG1, and IgG4 isotypes. SIT also prevents development of new sensitizations and progression of allergic rhinitis to asthma.