Expanded Regulatory T Cells Reduce Psoriatic Inflammation

Lymphocytes, computer artwork. T- and B-lymphocytes are part of the immune system. B cells mature in bone marrow and are responsible for humoral immunity; they operate by recognising a specific site (antigen) on the surface of a pathogen or foreign object, which they bind to before producing antibodies to destroy that antigen. T cells mature in the thymus and are involved in cell-mediated immunity, which does not rely on antibodies to fight antigens, but rather the activation of other immune cells. Interaction between B and T cells can increase B cell antibody production.
Researchers sought to explore whether and how dimerized translationally controlled tumor protein and dTCTP-binding peptide 2 function in the development of imiquimod-induced psoriatic skin inflammation.

Extracellular dimerized translationally controlled tumor protein (dTCTP) selectively suppressed regulatory T (Treg) cells that contribute to psoriatic inflammation and functional inhibition of dTCTP by dTCTP-binding peptide 2 (dTBP2) maintained immune homeostasis and attenuated inflammatory skin diseases via the expansion of Treg cells in laboratory mice, according to study findings published in Biomedicine & Pharmacotherapy.

Promoting immune cell activation as a pro-inflammatory cytokine, dTCTP plays a key role in the development of such allergic diseases as rhinitis and asthma. It is well-known that psoriasis is a chronic skin inflammation caused by a dysfunctional immune system, which, in turn, produces systemic inflammation in various organs and tissues.

Psoriatic inflammation is characterized by the increased infiltration of such effector T helper (Th) cells as Th1 and Th17, along with macrophages and impaired activity of Treg cells in the skin. It is thus important to prevent and treat psoriasis by the regulation of immune homeostasis through suppression of hyperactivated Th17 cell response and stimulation of impaired Treg cell function.

Based on the pro-inflammatory cytokine-like activity of dTCTP and the anti-inflammatory effect of dTBP2, the researchers sought to explore whether and how dTCTP and dTBP2 function in the development of imiquimod (IMQ)-induced psoriatic skin inflammation.

Topical application of (IMQ) was shown to increase inflammation in the skin of the back and the right ear, as observed with “expanded dermal vasculature, increased immune cell infiltration, and significant thickening of the back skin and ear.” Body weight decreased substantially and the spleen was enlarged in IMQ-treated mice.

Notably, TCTP was increased significantly in inflamed skin and in certain immune cells (ie, T cells, B cells, and macrophages) following IMQ treatment and was secreted into the serum to undergo dimerization. Extracellular dTCTP treatment selectively suppressed Treg cells, but not other effector Th cells, and also increased M1 macrophages. Further, dTBP2 inhibited dTCTP-mediated Treg suppression and stimulated expression of Treg cell markers in the spleen, and well as in inflammatory skin lesions.

The study was limited in that TCTP was identified only in IMQ-treated BALB/c mice, thus making it necessary to characterize whether dTCTP can be a good therapeutic target in other psoriatic models and in human psoriasis, as well.

The study authors concluded that the findings from the current study are suggestive of a “positive association between TCTP expression and pathogenic psoriasis.” Additional exploration of these results is warranted.


Cho H, Je JH, Kang J, et al. Dimeric translationally controlled tumor protein-binding peptide 2 attenuates imiquimod-induced psoriatic inflammation through induction of regulatory T cells. Biomed Pharmacother. Published online June 8, 2022. doi:10.1016/j.biopha.2022.113245