Peripheral Blood T Lymphocyte Subsets in Ulcerative Colitis

Ulcerative colitis (UC) is an idiopathic, chronic inflammatory disease of the large intestine, frequently involving the rectum, and characterized by chronic and recurrent mucosal inflammation and ulceration. Although its cause is not well understood, current evidence suggests innate and adaptive immunity play critical roles in its pathogenesis.

One of the main classes of immune cells that are affected by and contribute to UC is T cells. T-lymphocytes comprise a complex collection of highly differentiated T-cell subsets playing key roles in the regulation and the effector phase of the immune response. CD4+ T cells were found over-activated and proliferated in UC patients, which can induce disorders of the cytokine network and increase the occurrence of colitis.

Once intestinal pathogens or inflammatory mediators are not cleared in time, pro-inflammatory mononuclear phagocytes (MNPs) or polymorphonuclear leukocytes (PMNs) are often recruited to promote the polarization of naive CD4+ T cells into Th1, Th2, Th17, Treg and other subsets of cells.

The balances Th17/ Treg cells are important for maintaining intestinal homeostasis. Once the proportion Th17 cells increases, it often induces the production of pro-inflammatory cytokines that promote colonic inflammation, whereas Treg cells are usually secrete interleukin-10 (IL-10) and transforming growth factor-β (TGF-β) for anti-inflammatory regulations.

UC-associated inflammation is also characterized by huge number of activated B cells and plasma cells, the latter being involved in the production of cytotoxic granules, immunoglobulins, and various autoantibodies, Recent studies have highlighted a novel autoantibody against integrin αvβ6 in the serum of patients diagnosed with UC.