Toll-like receptor-mediated upregulation of CXCL16 in psoriasis orchestrates neutrophil activation

Innate immune processes are central in the development of the chronic inflammatory skin disease psoriasis. Studying stimulation of keratinocytes, monocytes and dendritic cells by type I interferons or ligation of toll-like receptors TLR1/2, TLR2/6 or TLR7, but not TLR7/8, resulted in enhanced surface expression and secretion of the chemokine CXCL16. The corresponding receptor CXCR6 was expressed on neutrophils whose recruitment into skin is important especially in early psoriatic disease. Using the recently developed technique real-time deformability cytometry demonstrated that CXCL16 and IL-8 decreased the stiffness and enhanced deformation of neutrophils facilitating transmigration through vessel wall.

Source: Journal of Investigative Dermatology - September 20, 2017 Category: Dermatology Authors: Sabine Steffen, Susanne Abraham, Maik Herbig, Franziska Schmidt, Kristin Blau, Susann Meisterfeld, Stefan Beissert, Jochen Guck, Claudia G ünther Tags: Original Article Source Type: research