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Mediators of Inflammation
Volume 2016, Article ID 6131234, 7 pages
Research Article

Th17 Cell Response in Mice following Motor Nerve Injury

1Oncology Research Institute, Loyola University Chicago, Maywood, IL 60153, USA
2Research Service, Department of Veterans Affairs, Edward Hines, Jr. VA Hospital, Hines, IL 60141, USA
3Department of Brain Disease, Gansu Province Chinese Traditional Medicine Hospital, Lanzhou, Gansu 730050, China
4Department of Ophthalmology, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA
5Department of Molecular Virology, Immunology & Medical Genetics, College of Medicine, The Ohio State University, Columbus, OH 43210, USA
6Department of Anatomy and Cell Biology, School of Medicine, Indiana University, Indianapolis, IN 46202, USA
7Research and Development Service, Roudebush VA Hospital, Indianapolis, IN 46202, USA
8Department of Otolaryngology, Loyola University Medical Center, Maywood, IL 60153, USA
9Department of Molecular Pharmacology and Therapeutics, Loyola University Chicago, Maywood, IL 60153, USA

Received 2 December 2015; Accepted 22 February 2016

Academic Editor: Jens Geginat

Copyright © 2016 Allen Ni 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.


An increased risk of ALS has been reported for veterans, varsity athletes, and professional football players. The mechanism underlying the increased risk in these populations has not been identified; however, it has been proposed that motor nerve injury may trigger immune responses which, in turn, can accelerate the progression of ALS. Accumulating evidence indicates that abnormal immune reactions and inflammation are involved in the pathogenesis of ALS, but the specific immune cells involved have not been clearly defined. To understand how nerve injury and immune responses may contribute to ALS development, we investigated responses of CD4+ T cell after facial motor nerve axotomy (FNA) at a presymptomatic stage in a transgenic mouse model of ALS (B6SJL ). mice, compared with WT mice, displayed an increase in the basal activation state of CD4+ T cells and higher frequency of Th17 cells, which were further enhanced by FNA. In conclusion, mice exhibit abnormal CD4+ T cell activation with increased levels of Th17 cells prior to the onset of neurological symptoms. Motor nerve injury exacerbates Th17 cell responses and may contribute to the development of ALS, especially in those who carry genetic susceptibility to this disease.