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Table 3 Therapeutic actions of regulatory T cell (Treg)s in allergic diseases

From: Subsets of regulatory T cells and their roles in allergy

Therapy Action of Tregs
SIT Suppression of T cell responses to the T-cell epitopes of major allergens. Autocrine action of IL-10 and/or TGF-β, which are produced by antigen-specific Tregs. They may suppress IgE production and induce IgG4 and IgA production against allergens [65]. Histamine released from mast cells and basophils may efficiently contribute to immunoregulation, and affect Tregs [6]. Der p immunotherapy causes increased number of Treg cells, and elevated IL-10 production. IL-10(+) Tregs may respond to Der p-2 and down-regulate NF-κB/p65 expression in PBMC to maintain immune tolerance during SIT [66].
SLIT Allergen extracts administered via the sublingual route are long retained at mucosal level, where the allergen molecules are captured by DCs, following their migration in the draining lymph nodes, presented to T cells to generate iTregs [64]. SLIT causes the absence of effectors cells, such as mast cells, basophils and eosinophils in the oral mucosa of allergic subjects. Skewing of allergic-specific effector T cells to a Tr1 phenotype appears to be a critical event in successful allergen-specific immunotherapy and glucocorticoids and beta2-agonists treatment [8].
Bacteria therapy Lactobacilli prime of DCs to drive the development of Tregs. These Tregs produce increased IL-10 inhibiting the proliferation of bystander T cells [4].
Treg therapy Transfer of OVA peptide-specific CD4 + CD25+ Tregs to OVA-sensitized mice reduces AHR, recruitment of eosinophils, and Th2 cytokine expression in the lung after allergen challenge [70].
  1. SIT = specific immunotherapy; Der p = Dermatophagoides pteronyssinus; PBMC = peripheral blood mononuclear cells; SLIT = sublingual immunotherapy; AHR = airway hyperresponsiveness; OVA = ovalbumin.