Th17 Cell Response in SOD1G93A Mice following Motor Nerve Injury
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, c...
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| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2016/6131234 |
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| _version_ | 1832551556108517376 |
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| author | Allen Ni Tao Yang Nichole A. Mesnard-Hoaglin Rafael Gutierrez Evan B. Stubbs Susan O. McGuire Virginia M. Sanders Kathryn J. Jones Eileen M. Foecking Junping Xin |
| author_facet | Allen Ni Tao Yang Nichole A. Mesnard-Hoaglin Rafael Gutierrez Evan B. Stubbs Susan O. McGuire Virginia M. Sanders Kathryn J. Jones Eileen M. Foecking Junping Xin |
| author_sort | Allen Ni |
| collection | DOAJ |
| description | 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 SOD1G93A). SOD1G93A 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, SOD1G93A 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. |
| format | Article |
| id | doaj-art-a4f184e211844aadbd6ac41aa10b6c1c |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-a4f184e211844aadbd6ac41aa10b6c1c2025-02-03T06:01:10ZengWileyMediators of Inflammation0962-93511466-18612016-01-01201610.1155/2016/61312346131234Th17 Cell Response in SOD1G93A Mice following Motor Nerve InjuryAllen Ni0Tao Yang1Nichole A. Mesnard-Hoaglin2Rafael Gutierrez3Evan B. Stubbs4Susan O. McGuire5Virginia M. Sanders6Kathryn J. Jones7Eileen M. Foecking8Junping Xin9Oncology Research Institute, Loyola University Chicago, Maywood, IL 60153, USADepartment of Brain Disease, Gansu Province Chinese Traditional Medicine Hospital, Lanzhou, Gansu 730050, ChinaResearch Service, Department of Veterans Affairs, Edward Hines, Jr. VA Hospital, Hines, IL 60141, USAOncology Research Institute, Loyola University Chicago, Maywood, IL 60153, USAResearch Service, Department of Veterans Affairs, Edward Hines, Jr. VA Hospital, Hines, IL 60141, USAResearch Service, Department of Veterans Affairs, Edward Hines, Jr. VA Hospital, Hines, IL 60141, USADepartment of Molecular Virology, Immunology & Medical Genetics, College of Medicine, The Ohio State University, Columbus, OH 43210, USADepartment of Anatomy and Cell Biology, School of Medicine, Indiana University, Indianapolis, IN 46202, USAResearch Service, Department of Veterans Affairs, Edward Hines, Jr. VA Hospital, Hines, IL 60141, USAOncology Research Institute, Loyola University Chicago, Maywood, IL 60153, USAAn 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 SOD1G93A). SOD1G93A 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, SOD1G93A 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.http://dx.doi.org/10.1155/2016/6131234 |
| spellingShingle | Allen Ni Tao Yang Nichole A. Mesnard-Hoaglin Rafael Gutierrez Evan B. Stubbs Susan O. McGuire Virginia M. Sanders Kathryn J. Jones Eileen M. Foecking Junping Xin Th17 Cell Response in SOD1G93A Mice following Motor Nerve Injury Mediators of Inflammation |
| title | Th17 Cell Response in SOD1G93A Mice following Motor Nerve Injury |
| title_full | Th17 Cell Response in SOD1G93A Mice following Motor Nerve Injury |
| title_fullStr | Th17 Cell Response in SOD1G93A Mice following Motor Nerve Injury |
| title_full_unstemmed | Th17 Cell Response in SOD1G93A Mice following Motor Nerve Injury |
| title_short | Th17 Cell Response in SOD1G93A Mice following Motor Nerve Injury |
| title_sort | th17 cell response in sod1g93a mice following motor nerve injury |
| url | http://dx.doi.org/10.1155/2016/6131234 |
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