<unk>  is a specific marker of natural T regulatory cells (nTregs, a lineage of T cells) and adaptive/induced T regulatory cells (a/iTregs), also identified by other less specific markers such as CD25 or CD45RB. In animal studies, Tregs that express<unk>  are critical in the transfer of immune tolerance, especially self-tolerance. The induction or administration of<unk>  positive T cells has, in animal studies, led to marked reductions in (autoimmune) disease severity in models of diabetes, multiple sclerosis, asthma, inflammatory bowel disease, thyroiditis and renal disease. Human trials using regulatory T cells to treat graft-versus-host disease have shown efficacy. Further work has shown that T cells are more plastic in nature than originally thought. This means that the use of regulatory T cells in therapy may be risky, as the T regulatory cell transferred to the patient may change into T helper 17 (Th17) cells, which are pro-inflammatory rather than regulatory cells. Th17 cells are proinflammatory and are produced under similar environments as a/iTregs. Th17 cells are produced under the influence of TGF-β and IL-6 (or IL-21), whereas a/iTregs are produced under the influence of solely TGF-β, so the difference between a proinflammatory and a pro-regulatory scenario is the presence of a single interleukin. IL-6 or IL-21 is being debated by immunology laboratories as the definitive signaling molecule. Murine studies point to IL-6 whereas human studies have shown IL-21.<unk>  is the major transcription factor controlling T-regulatory cells (Treg or CD4+ cells). CD4+ cells are leukocytes responsible for protecting animals from foreign invaders such as bacteria and viruses. Defects in this gene's ability to function can cause IPEX syndrome (IPEX), also known as X-linked autoimmunity-immunodeficiency syndrome as well as numerous cancers. While CD4+ cells are heavily regulated and require multiple transcription factors such as STAT-5 and AhR in order to become active and function properly,<unk>  has been identified as the master regulator for Treg lineage.<unk>  can either act as a transcriptional activator or suppressor depending on what specific transcriptional factors such as deacetylases and histone acetylases are acting on it. The<unk>  gene is also known to convert naïve T-cells to Treg cells, which are capable of an in vivo and in vitro suppressive capabilities suggesting that<unk>  is capable of regulating the expression of suppression-mediating molecules. Clarifying the gene targets of<unk>  could be crucial to the comprehension of the suppressive abilities of Treg cells.
FOXP3
FOXC2
FOXF1
Mad2
SOX2
CDK13
INK4
TFM-4AS-1