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BioMed Research International
Volume 2015, Article ID 189638, 10 pages
Research Article

CCL27: Novel Cytokine with Potential Role in Pathogenesis of Multiple Sclerosis

1Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Tatarstan 420008, Russia
2Department of Biochemistry and Molecular Biology, University of Nevada School of Medicine, Reno, NV 89557, USA
3WP Institute, Reno, NV 89557, USA
4Kazan State Medical University, 49 Butlerova Street, Kazan, Tatarstan 420012, Russia
5Excellence Cluster Cardio-Pulmonary System, Justus Liebig University, Aulweg 130, 35392 Giessen, Germany

Received 7 November 2014; Accepted 11 December 2014

Academic Editor: András Palotás

Copyright © 2015 Svetlana F. Khaiboullina et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Multiple sclerosis (MS) is an autoimmune and neurodegenerative disease of unknown etiology. Leukocyte infiltration of brain tissue and the subsequent inflammation, demyelination, axonal damage, and formation of sclerotic plaques is a hallmark of MS. Upregulation of proinflammatory cytokines has been suggested to play an essential role in regulating lymphocyte migration in MS. Here we present data on serum cytokine expression in MS cases. Increased serum levels of IL-17 and IL-23 were observed, suggesting activation of the Th17 population of immune effector cells. Additionally, increased levels of IL-22 were observed in the serum of those with acute phase MS. Unexpectedly, we observed an upregulation of the serum chemokine CCL27 in newly diagnosed and acute MS cases. CCL27 is an inflammatory chemokine associated with homing of memory T cells to sites of inflammation. Therefore, its upregulation in association with MS suggests a potential role in disease pathogenesis. Our data supports previous reports showing IL-17 and -23 upregulation in association with MS and potentially identify a previously unknown involvement for CCL27.