Abstract
Regulatory T cells (Tregs) are key mediators of peripheral self-tolerance and alterations in their frequencies, stability, and function have been linked to autoimmunity. The antigen-specific induction of Tregs is a long-envisioned goal for the treatment of autoimmune diseases given reduced side effects compared to general immunosuppressive therapies. However, the translation of antigen-specific Treg inducing therapies for the treatment or prevention of autoimmune diseases into the clinic remains challenging. In this mini review, we will discuss promising results for antigen-specific Treg therapies in allergy and specific challenges for such therapies in autoimmune diseases, with a focus on type 1 diabetes (T1D). We will furthermore discuss opportunities for antigen-specific Treg therapies in T1D, including combinatorial strategies and tissue-specific Treg targeting. Specifically, we will highlight recent advances in miRNA-targeting as a means to foster Tregs in autoimmunity. Additionally, we will discuss advances and perspectives of computational strategies for the detailed analysis of tissue-specific Tregs on the single-cell level.
Highlights
The body’s immune system has evolved to effectively defeat and destroy infiltrating foreign pathogens
With the goal to understand mechanisms of impaired Treg induction, we focused on microRNAs. miRNAs are small non-coding RNAs that can sequence- inhibit their target mRNAs. miRNAs usually target a multitude of different mRNAs, thereby regulating entire signaling pathways and complex cellular states, such as T cell activation, which makes them important targets for immunotherapies [26,27,28]
In line with excessive T cell activation observed during recent onset of islet autoimmunity, we found miRNA181a-5p to be increased in CD4+ T cells from peripheral blood of children with recent activation of islet autoimmunity
Summary
The body’s immune system has evolved to effectively defeat and destroy infiltrating foreign pathogens. The ability of Tregs to regulate immune responses via direct inhibition of effector T cells with the same specificity and via modulation of antigen-presenting cell (APCs), a process called bystander suppression, makes Tregs an important target for tolerizing therapies [12].
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