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Inhibition of IL-17 and IL-23 in Human Keratinocytes by the A 3 Adenosine Receptor Agonist Piclidenoson

Inhibition of IL-17 and IL-23 in Human Keratinocytes by the A 3 Adenosine Receptor Agonist Piclidenoson

Shira Cohen, Faina Barer, Inbal Itzhak, Michael H Silverman, Pnina Fishman

J Immunol Res. 2018 May 15;2018:2310970.

PMID: 29862305

Abstract:

Interleukin-17 and interleukin-23 play major roles in the inflammatory process in psoriasis. The Gi protein-associated A3 adenosine receptor (A3AR) is known to be overexpressed in inflammatory cells and in peripheral blood mononuclear cells (PBMCs) of patients with autoimmune inflammatory conditions. Piclidenoson, a selective agonist at the A3AR, induces robust anti-inflammatory effect in psoriasis patients. In this study, we aimed to explore A3AR expression levels in psoriasis patients and its role in mediating the anti-inflammatory effect of piclidenoson in human keratinocyte cells. A3AR expression levels were evaluated in skin tissue and PBMCs derived from psoriasis patients and healthy subjects. Proliferation assay and the expression of signaling proteins were used to evaluate piclidenoson effect on human keratinocytes (HaCat). High A3AR expression levels were found in a skin biopsy and in PBMCs from psoriasis patients in comparison to healthy subjects. Piclidenoson inhibited the proliferation of HaCat cells through deregulation of the NF-κB signaling pathway, leading to a decrease in interleukin-17 and interleukin-23 expression levels. This effect was counteracted by the specific antagonist MRS 1523. A3AR overexpression in skin and PBMCs of psoriasis patients may be used as a target to inhibit pathological cell proliferation and the production of interleukin-17 and interleukin-23.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP212329378	MRS 1523		212329-37-8	Price

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