Abstract
The immune system regulates itself to establish an appropriate immune response to potentially harmful pathogens while tolerating harmless environmental antigens and self-antigens. A central role in this balance is played by regulatory T cells (Tregs) through various ways of actions. By means of molecule secretion and cell-cell contact mechanisms, Tregs may have the capacity to modulate effector T cells and suppress the action of proinflammatory cytokines across a broad range of cell types. As a result, abnormal regulatory T cell function has been pointed as a main cause in the development of allergic diseases, a major public health problem in industrialized countries, with a high socioeconomic impact. This prevalence and impact have created an international interest in improving the allergy diagnosis and therapy. Additionally, research has sought to gain a better understanding of the molecular mechanisms underlining this kind of disease, in order to a better management. At this respect, the role of Treg cells is one of the most promising areas of research, mainly because of their potential use as new immunotherapeutical approaches. Therefore, the aim of this review is to update the existing knowledge of the role of Tregs in this pathology deepening in their implication in allergen-specific therapy (AIT).
Highlights
Current Knowledge about Treg CellsThe immune system (IS) requires tight control to protect the organism from exaggerated stimulatory signals triggered by harmless antigens, such as self-antigens and environmental substances
Though this review focuses on the function of the Tregs, it is important to keep in mind that these cells do not work in Journal of Immunology Research isolation
The junction ligand-receptor produces signaling by phosphorylation of some proteins that induce the activation of signal transducer and activator of transcription 3 (STAT3), which induce the expression of suppressor of cytokine signaling 3 (SOCS3) and several preapoptotic genes, as well as the inhibition in the production of proinflammatory cytokines such as TNF-α
Summary
The immune system (IS) requires tight control to protect the organism from exaggerated stimulatory signals triggered by harmless antigens, such as self-antigens and environmental substances. Years later [35], it was described how USP21 stabilizes the FOXP3 protein by mediating its deubiquitination and controls Treg lineage stability in vivo Another regulator proposed was SOCS2, a suppressor of cytokine signaling (SOCS) proteins, which inhibits the development of Th2 cells and allergic immune responses. The main mechanisms of Treg action include regulatory cytokine production such as IL-10, IL-35, and TGF-β; the metabolic disruption mechanisms: CD25, cAMP, histamin receptor 2, adenosine receptor 2, CD39, and CD73; mechanisms with targets in DCs such as cytotoxic T lymphocyte antigen-4 (CTLA-4), program death-1 (PD-1), and cytolysis mechanism (granzymes A and B) [14, 46, 47] As detailed above, it has been described how the suppressive functions of Tregs are induced under inflammatory conditions by the specific expression of receptors and transcription factors. This is another point justifying Tregs as excellent candidates for regulating allergic diseases
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