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Int. J. Mol. Sci. 2017, 18(5), 1000; doi:10.3390/ijms18051000

Interleukin 17A Promotes Lymphocytes Adhesion and Induces CCL2 and CXCL1 Release from Brain Endothelial Cells

Department of Neurology and Stroke, Medical University of Lodz, Zeromskiego 113, 90-549 Lodz, Poland
These authors contributed equally to this work.
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Author to whom correspondence should be addressed.
Academic Editor: Richard L. Hoover
Received: 21 February 2017 / Revised: 31 March 2017 / Accepted: 1 May 2017 / Published: 8 May 2017
(This article belongs to the Special Issue Cell-cell Interactions in Blood Vessels)
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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). Tumor necrosis factor alpha (TNF-α) or interleukin 17 (IL-17) stimulation is known to enhance the adherence of Th17 cells to the brain endothelium. The brain endothelial cells (bEnd.3) express Vascular cell adhesion molecule 1 (VCAM-1), the receptor responsible for inflammatory cell adhesion, which binds very late antigen 4 (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-α 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 observation may suggest potential therapeutic targets for the prevention of autoimmune neuroinflammation development in the CNS. View Full-Text
Keywords: Th17 cells; blood–brain barrier; chemokines; VCAM-1; neuroinflammation; multiple sclerosis Th17 cells; blood–brain barrier; chemokines; VCAM-1; neuroinflammation; multiple sclerosis
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MDPI and ACS Style

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.

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