Colonic regulatory T cells (cTregs)

Colonic regulatory T cells (cTregs) are a specialized subset of CD4+ FOXP3+ T cells that are essential for maintaining immune homeostasis and preventing excessive inflammation in the gut [1]. Unlike systemic Tregs, a significant portion of cTregs are induced peripherally in response to signals from the gut microbiota, particularly short-chain fatty acids like butyrate [2, 3]. These cells are often characterized by the expression of the transcription factor RORγt, which is required for their suppressive function against intestinal inflammation [4]. In diseases such as Ulcerative Colitis and Crohn's Disease, the frequency or function of cTregs is often impaired, leading to a loss of tolerance toward commensal bacteria [5]. Conversely, in colorectal cancer, cTregs can accumulate in the tumor microenvironment and suppress anti-tumor immune responses, thereby promoting tumor growth [6]. Therapeutic strategies include the use of low-dose IL-2 to expand Treg populations, microbiota-based therapies to induce cTregs, or monoclonal antibodies like Vedolizumab that affect the trafficking of T cells to the colonic mucosa [7, 8].

Other names

Colonic TregsGut-resident regulatory T cellsIntestinal FOXP3+ T cellsRORγt+ regulatory T cells

Therapeutic modulation involves the expansion of the Treg pool, enhancement of suppressive cytokine production (e.g., IL-10), or the inhibition of gut-specific homing receptors like integrin alpha-4 beta-7.