Preprint Article Version 1 This version is not peer-reviewed

Th17 Cells Interactions with the Brain Endothelium in Vitro

These authors contributed equally to this work.
Version 1 : Received: 14 March 2017 / Approved: 15 March 2017 / Online: 15 March 2017 (07:34:02 CET)

A peer-reviewed article of this Preprint also exists.

Wojkowska, D.W.; Szpakowski, P.; Glabinski, A. Interleukin 17A Promotes Lymphocytes Adhesion and Induces CCL2 and CXCL1 Release from Brain Endothelial Cells. Int. J. Mol. Sci. 2017, 18, 1000. Wojkowska, D.W.; Szpakowski, P.; Glabinski, A. Interleukin 17A Promotes Lymphocytes Adhesion and Induces CCL2 and CXCL1 Release from Brain Endothelial Cells. Int. J. Mol. Sci. 2017, 18, 1000.

Journal reference: Int. J. Mol. Sci. 2017, 18, 1000
DOI: 10.3390/ijms18051000

Abstract

The nature of the interaction between Th17 cells and the blood-brain barrier (BBB) is critical for the development of autoimmune inflammation in the central nervous system (CNS). TNF-a or IL-17 stimulation is known to enhance the adherence of Th17 cells to the brain endothelium. The brain endothelial cells (bEnd.3) express VCAM-1, the receptor responsible for inflammatory cell adhesion, which binds VLA-4 on migrating effector lymphocytes at the early stage of brain inflammation. The present study examines the effect of the pro-inflammatory cytokines TNF-a and IL-17 on the adherence of Th17 cells to bEnd.3 The bEnd.3 cells were found to increase production of CCL2 and CXCL1 after stimulation by pro-inflammatory cytokines, while CCL2, CCL5, CCL20 and IL17 induced Th17 cell migration through a bEnd.3 monolayer. This interaction between Th17 cells and the brain endothelium appears to be mediated by VCAM-1 and some chemotactic cytokines. This observation may suggest potential therapeutic targets for the prevention of autoimmune neuroinflammation development in the CNS.

Subject Areas

Th17 cells; blood - brain barrier; chemokines; VCAM-1; neuroinflammation; multiple sclerosis

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