Autoreactive T-Cells in Psoriasis: Are They Spoiled Tregs and Can Therapies Restore Their Functions?

Area of Science:

• Immunology
• Dermatology
• Cell Biology

Background:

• Psoriasis is a chronic inflammatory skin disease affecting 2-4% globally.
• The disease is characterized by T-cell derived factors like Th17 and Th1 cytokines, and IL-23.
• An autoimmune component involves autoreactive T-cells targeting self-antigens like LL37 and keratins.

Purpose of the Study:

• To review current findings on regulatory T-cells (Tregs) in psoriasis.
• To discuss Treg function, potential conversion to T-effector cells, and therapeutic implications.
• To present experimental data on T-cells specific for the autoantigen LL37.

Main Methods:

• Narrative review of existing literature on Tregs in psoriasis.
• Analysis of Treg numbers and function in psoriatic skin and circulation.
• Experimental investigation of T-cells recognizing the autoantigen LL37.

Main Results:

• Tregs are increased in psoriasis but exhibit impaired regulatory/suppressive function.
• Evidence suggests Tregs may convert into pathogenic T-effector cells, such as Th17 cells, under inflammation.
• Experimental data indicate potential shared specificity between Tregs and autoreactive T-cells for LL37.

Conclusions:

• Psoriasis pathogenesis involves impaired Treg function, possibly due to conversion to effector cells.
• Therapies targeting psoriasis may need to restore Treg numbers and suppressive functions.
• Restoring Treg homeostasis is a potential therapeutic strategy for psoriasis management.