Regulatory T cells (Tregs) are a subset of T lymphocytes that prevent autoimmune reactions and suppress excessive immune responses. Tregs develop within the thymus, where other conventional T cells mature, from a distinct lineage of precursor cells that express the transcription factor Foxp3, essential for Treg development. Thymocytes expressing Foxp3 become committed to the Treg lineage with commitment also influenced by the transcription factors Runx1 and Runx3, and cytokines TGF-β, IL-2 and IL-10. Tregs that successfully develop in the thymus have a high affinity for self-antigens. This is crucial for their ability to prevent autoimmune reactions, as they can suppress the activation and expansion of self-reactive T cells. Tregs employ various mechanisms to exert their suppressive effects, helping to prevent autoimmune diseases and maintain immune tolerance. Tregs can directly interact with and suppress the function of other immune cells, such as effector T cells and antigen-presenting cells (APCs). This is achieved through cell surface molecules like CTLA-4 (cytotoxic T lymphocyte-associated antigen 4) and PD-1 (programmed cell death protein 1), which inhibit co-stimulatory signals required for T cell activation. Tregs also produce anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β). These cytokines can inhibit the activation and proliferation of effector T cells and downregulate the inflammatory response of immune cells. In addition to cellular effects, Tregs also have distinct metabolic profiles that contribute to their suppressive function. They consume high levels of IL-2, limiting its availability for effector T cells. Tregs also express high levels of the IL-2 receptor (CD25) and readily titrate IL-2, a cytokine required for proliferation of other T cells. By depriving effector T cells of IL-2, Tregs limit their expansion and activity. Tregs can also inhibit the maturation and activation of antigen-presenting dendritic cells (DCs), which are crucial for initiating immune responses. By doing so, Tregs indirectly suppress the activation of other effector T cells. Tregs migrate to inflamed tissues and sites of immune activation. The recruitment of Tregs to sites of inflammation is controlled by a combination of chemotactic signals, adhesion molecules, and interactions with other immune cells. For example, chemokines such as CXCL9, CXCL12, CCL17 and CCL22 attract Treg cells to sites of inflammation, preventing excessive inflammation and tissue damage. Tregs can also influence B cell responses by inhibiting antibody production and class-switching, thereby suppressing humoral immune responses, and interact with and inhibit the activity of natural killer (NK) cells, which play a role in antiviral and antitumor responses. This contributes to the maintenance of immune tolerance. Tregs are also particularly important for controlling autoimmune reactions. They recognize self-reactive T cells and inhibit their activation, preventing them from attacking the body's own tissues and causing autoimmune diseases. Finally, Tregs play a critical role in transplant tolerance by suppressing the immune response against transplanted tissues, essential in preventing graft rejection after organ transplantation. In the context of cancer, Tregs can unfortunately also hinder anti-tumour immune responses by inhibiting the activation and function of tumour-targeting T cells, contributing to tumour immune evasion. We offer a wide product catalogue of research tools for investigating regulatory T cells, including CD45 antibodies, CD4 antibodies, CD3 antibodies, ICAM1 ELISA Kits, and Granzyme B ELISA Kits. Explore our full regulatory T cells product range below and discover more, for less.