TREX2 genes code for an endonuclease that maintains the stability of the entire genome, including repair mechanisms like DNA degradation. The gene seems to have a complicated role in the body; previous studies of mice lacking TREX2 showed them to be highly susceptible to ultraviolet light-induced carcinogenesis, and the present study provides evidence that the same gene is highly expressed in the skin of psoriasis patients.
“The release of several signals by skin cells that are dying contributes to the creation and spreading of the chronic immune response and hyper-proliferation and irregular differentiation of epidermis,” said first author Joan Manils. Using biopsies from humans with and without psoriasis along with mice models of psoriasis with both normal and deficient TREX2, Manils and the research team investigated the true function of TREX2 in cases of psoriasis.
They ultimately found that psoriasis skin cells had a high increase of TREX2 expression, mainly from the cell nuclei of keratinocytes, the most abundant cells on the skin, that are growing and dying abnormally.
With a clearer connection drawn between TREX2 and psoriasis, the researchers from the Universidad de Barcelona next plan to investigate the details surrounding the connection: the role of TREX2 in the development and maintenance of psoriasis.
"Most of the current treatments are aimed at blocking the action of the immune system and if they have good results, these treatments are chronic and involve the immune response of the sick person," said co-author Francisco Ciruela. However, in the future, a potential treatment for psoriasis could be to target TREX2, rather than the entire immune system.
Source: Universidad de Barcelona, National Psoriasis Foundation, Nature Methods