Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments
The Guillain-Barré syndrome (GBS) is considered a T helper 1 (Th1) cells-mediated acute inflammatory peripheral neuropathy. However, some changes in GBS could not be explained completely by Th1 cells pathogenic role. Recently, Th17 cells have been identified and can mediate tissue inflammation and a...
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| Format: | Article |
| Language: | English |
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Wiley
2014-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2014/740947 |
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| author | Shujuan Li Tao Jin Hong-Liang Zhang Hong Yu Fanhua Meng Hernan Concha Quezada Jie Zhu |
| author_facet | Shujuan Li Tao Jin Hong-Liang Zhang Hong Yu Fanhua Meng Hernan Concha Quezada Jie Zhu |
| author_sort | Shujuan Li |
| collection | DOAJ |
| description | The Guillain-Barré syndrome (GBS) is considered a T helper 1 (Th1) cells-mediated acute inflammatory peripheral neuropathy. However, some changes in GBS could not be explained completely by Th1 cells pathogenic role. Recently, Th17 cells have been identified and can mediate tissue inflammation and autoimmune response. Therefore, a study on the role of Th17 and Th22 cells and their cytokines in GBS is necessary for exploring the pathogenesis of GBS. Here, we detected the frequency of Th1, Th17, and Th22 cells by using 4-color flow cytometry and we detected the plasma levels of IL-17 and IL-22 by ELISA in GBS patients, relapsing-remitting multiple sclerosis patients at the acute phase of relapse, viral encephalitis or meningitis patients and healthy controls. Our data showed that the frequency of circulating Th1, Th17, and Th22 cells was significantly increased in GBS patients. The plasma levels of IL-17 and IL-22 in GBS and relapsing-remitting multiple sclerosis at the acute phase of relapse were also markedly elevated. Enhanced circulating Th22 cells were correlated with GBS severity. Intravenous immunoglobulin therapy downregulated Th17, and Th22 cells and the plasma levels of IL-17 and IL-22 in GBS patients. Th17 and Th22 cells may be involved in the pathogenesis of GBS, and intravenous immunoglobulin mediates therapeutic effects by downregulating these cells and their cytokines. |
| format | Article |
| id | doaj-art-88be69908a15463ca3a766e5d117d01e |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-88be69908a15463ca3a766e5d117d01e2025-02-03T01:12:56ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/740947740947Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg TreatmentsShujuan Li0Tao Jin1Hong-Liang Zhang2Hong Yu3Fanhua Meng4Hernan Concha Quezada5Jie Zhu6Department of Neurology, the First Hospital, Jilin University, Changchun 130021, ChinaDepartment of Neurology, the First Hospital, Jilin University, Changchun 130021, ChinaDepartment of Neurology, the First Hospital, Jilin University, Changchun 130021, ChinaDepartment of Neurobiology, Care Sciences and Society, Karolinska Institute, Karolinska University Hospital, Huddinge, 14186 Stockholm, SwedenDepartment of Neurology, the First Hospital, Jilin University, Changchun 130021, ChinaCenter for Infectious Medicine, Department of Medicine, Karolinska Institute, Karolinska University Hospital, Huddinge, 14186 Stockholm, SwedenDepartment of Neurology, the First Hospital, Jilin University, Changchun 130021, ChinaThe Guillain-Barré syndrome (GBS) is considered a T helper 1 (Th1) cells-mediated acute inflammatory peripheral neuropathy. However, some changes in GBS could not be explained completely by Th1 cells pathogenic role. Recently, Th17 cells have been identified and can mediate tissue inflammation and autoimmune response. Therefore, a study on the role of Th17 and Th22 cells and their cytokines in GBS is necessary for exploring the pathogenesis of GBS. Here, we detected the frequency of Th1, Th17, and Th22 cells by using 4-color flow cytometry and we detected the plasma levels of IL-17 and IL-22 by ELISA in GBS patients, relapsing-remitting multiple sclerosis patients at the acute phase of relapse, viral encephalitis or meningitis patients and healthy controls. Our data showed that the frequency of circulating Th1, Th17, and Th22 cells was significantly increased in GBS patients. The plasma levels of IL-17 and IL-22 in GBS and relapsing-remitting multiple sclerosis at the acute phase of relapse were also markedly elevated. Enhanced circulating Th22 cells were correlated with GBS severity. Intravenous immunoglobulin therapy downregulated Th17, and Th22 cells and the plasma levels of IL-17 and IL-22 in GBS patients. Th17 and Th22 cells may be involved in the pathogenesis of GBS, and intravenous immunoglobulin mediates therapeutic effects by downregulating these cells and their cytokines.http://dx.doi.org/10.1155/2014/740947 |
| spellingShingle | Shujuan Li Tao Jin Hong-Liang Zhang Hong Yu Fanhua Meng Hernan Concha Quezada Jie Zhu Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments Mediators of Inflammation |
| title | Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments |
| title_full | Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments |
| title_fullStr | Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments |
| title_full_unstemmed | Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments |
| title_short | Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments |
| title_sort | circulating th17 th22 and th1 cells are elevated in the guillain barre syndrome and downregulated by ivig treatments |
| url | http://dx.doi.org/10.1155/2014/740947 |
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