Abstract
Allergic diseases are chronic inflammatory disorders in which there is failure to mount effective tolerogenic immune responses to inciting allergens. The alarming rise in the prevalence of allergic diseases in recent decades has spurred investigations to elucidate the mechanisms of breakdown in tolerance in these disorders and means of restoring it. Tolerance to allergens is critically dependent on the generation of allergen-specific regulatory T (Treg) cells, which mediate a state of sustained non-responsiveness to the offending allergen. In this review, we summarize recent advances in our understanding of mechanisms governing the generation and function of allergen-specific Treg cells and their subversion in allergic diseases. We will also outline approaches to harness allergen-specific Treg cell responses to restore tolerance in these disorders.
Highlights
Regulatory T (Treg) cells play a key role in the maintenance of immunological self-tolerance and in restraining deleterious immune responses to both self and foreign antigens[1]
Sakaguchi et al originally described a population of CD4+ T cells expressing the cell surface marker CD25—interleukin-2 (IL-2) receptor alpha chain—that maintained peripheral immunological tolerance in mice
Additional Foxp3– Treg cell populations have been described[12], this review is focused on CD4+CD25+Foxp3+ Treg cells, the most well-characterized subset of Treg cells whose deficiency in both humans and mouse models precipitates lethal autoimmunity and inflammatory disorders
Summary
Regulatory T (Treg) cells play a key role in the maintenance of immunological self-tolerance and in restraining deleterious immune responses to both self and foreign antigens[1]. Derangement of antigen-specific Treg cell responses in allergic diseases Oral tolerance is associated with the development of iTreg cells from naïve CD4+ T cells that are activated in the presence of TGF-β1 and CD103+ classic dendritic cells in the gut that express interferon gamma regulatory factor 8 (IRF8) (Figure 2)[41,69]. Failure of MyD88-dependent signaling in Treg cells severely restricted the evolution of antigen-specific Treg cell responses in the gut, consistent with the action of microbiotic products through innate immune signaling mechanisms in Treg cells promoting their expansion and function[111] The loss of these and other mechanisms through dysbiosis may compromise the development of Treg cells in FA and other gut dysbiotic disorders. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
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