Immunomodulatory Effects of Regulatory T Cells (Treg) and Treg-Derived Extracellular Vesicles

Regulatory T cells (Tregs) are a specialized subpopulation of T cells that work to suppress the immune response, maintaining balance and self-tolerance. Tregs exert their suppressive effects through various mechanisms, including inhibiting the proliferation and function of effector T cells, secreting immunosuppressive cytokines such as IL-10 and TGF-beta, and interacting with other immune cells and tissues. Their ability to modulate immune responses makes them a promising target for therapeutic interventions in conditions characterized by dysregulated immunity.

Treg-derived extracellular vesicles (Treg-EVs) have similar immunosuppressive ability to their parent cells. It is a well-known fact that the tumor microenvironment favors cancer progression, and Treg-derived exosomes play a significant role in aiding this fact. Treg-EVs express specific molecules (similar to their parent cells) and deliver cargoes as a novel contact-independent mechanism of immune modulation. Since Treg-EVs have an immuno-modulatory effect, they can have a far-reaching impact on a diverse range of diseases.

The aim of this Research Topic is to focus on the immuno-modulatory properties of regulatory T cells and Treg-derived extracellular vesicles. Given their capacity to modulate immune responses, Tregs and Treg-derived exosomes present a compelling target for therapeutic interventions in conditions characterized by immune dysregulation.

This Research Topic will explore the intricate immunomodulatory mechanisms of Tregs and extracellular vesicles derived from Treg cells and their far-reaching impact on a diverse range of diseases. We are also seeking submissions that delve into the potential therapeutic applications of the valuable insights gleaned from these extracellular vesicles. Tregs and Treg-EVs are crucial for maintaining the body's immune tolerance and share many molecular signaling pathways with conventional T cells, including cytotoxic T cells, which are the primary mediators of tumor immunity. Therefore, the challenge lies in the inability to specifically target and neutralize Tregs/Treg-EVs in the tumor microenvironment without globally compromising self-tolerance.

Articles focusing on advances in characterizing Treg-EVs, with an emphasis on the functional roles of costimulatory and inhibitory receptors in Tregs, as well as the evaluation of Treg-EVs as potential clinical targets, are also welcome.