Depletion of JunB in the Skin Causes Psoriasis-Like Disease and Arthritis

Title: Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins.
: Zenz R, et al.
Publication: Nature. 2005 Sep 15;437(7057):369-75.

The authors reported that in psoriatic lesion, epidermal keratinocytes (skin cells that produce keratin tissue) had decreased expression of JunB gene, which had been genetically mapped to the psoriasis susceptibility region PSORS6.

In an experiment, depletion of JunB and its companion c-Jun in adult mice resulted in symptoms of psoriasis, including arthritic lesion within 2 weeks.

For the development of arthritic lesion, T and B cells as well as signaling through tumor necrosis factor receptor 1 (TNFR 1) were required. The authors noted that prior to the onset of the disease, two chemotactic proteins S100A8 and S100A9 were previously mapped to psoriasis susceptibility region PSORS4. These proteins were strongly induced in mutant keratinocyte cells.

The authors proposed that the depletion of JunB/activator protein 1 (AP-1) in keratinocyte trigger a chemokine/cytokine expression (a type of immune response), which in turn result in localization of neutrophils and macrophages to the skin thus resulting in psoriasis symptoms.

The authors suggested that these changes in the skin were sufficient to initiate both the skin lesion and the arthritis or joint pain in psoriasis.

Editor’s Note: chemotactic proteins are proteins that are involved in movement or cells along a chemical concentration gradient, either toward or away from a chemical source.

Cytokine is a type of regulatory proteins that are released by cells of the immune system as regulator of immune response. Chemokine is a type of cytokine involved in inflammation. Neutrophil is a type of white blood cell that can destroy microorganisms during an immune reaction. Macrophage is a large cell that can engulf or swallow and destroy foreign substances in the body.

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