scholarly journals Circulating Th17, Th22, and Th1 Cells Are Elevated in the Guillain-Barré Syndrome and Downregulated by IVIg Treatments

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Shujuan Li ◽  
Tao Jin ◽  
Hong-Liang Zhang ◽  
Hong Yu ◽  
Fanhua Meng ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Intravenous Immunoglobulin ◽  
Acute Phase ◽  
Plasma Levels ◽  
Guillain Barre Syndrome ◽  
Th1 Cells ◽  
Th22 Cells ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Relapsing Remitting Multiple Sclerosis

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.

scholarly journals Elevated sCD40L in Secondary Progressive Multiple Sclerosis in Comparison to Non-progressive Benign and Relapsing Remitting Multiple Sclerosis

2021 ◽  
Vol 13 ◽  
pp. 117957352110507
Author(s):  
Qi Wu ◽  
Qin Wang ◽  
Jennifer Yang ◽  
Jacob WS Martens ◽  
Elizabeth A Mills ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Disease Progression ◽  
Plasma Levels ◽  
Disease Onset ◽  
Progressive Multiple Sclerosis ◽  
Secondary Progressive Multiple Sclerosis ◽  
Secondary Progressive ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Relapsing Remitting Multiple Sclerosis

Background: The long-term prognosis of relapsing-remitting multiple sclerosis (RRMS) is usually unfavorable as most patients transition to secondary progressive multiple sclerosis (SPMS) with accumulative disability. A rare form of non-progressive multiple sclerosis (MS) also exists, known as benign MS (BMS or NPMS), which lacks disease progression defined as Expanded Disability Status Scale (EDSS) ≤3 after 15 years of disease onset without treatment. Purpose: Our study aims to identify soluble plasma factors predicting disease progression in multiple sclerosis (MS). Research Design and Study Sample: We utilized Luminex multiplex to analyze plasma levels of 33 soluble factors, comparing 32 SPMS patients to age-, sex-, and disease duration-matched non-progressive BMS patients, as well as to RRMS patients and healthy controls. Results: Plasma levels of EGF, sCD40L, MCP1/CCL2, fractalkine/CX3CL1, IL-13, Eotaxin, TNFβ/LTα, and IL-12p40 were significantly different between the various types of MS. Plasma sCD40L was significantly elevated in SPMS compared to BMS and RRMS. The combination of MCP1/CCL2 and sCD40L discriminated between RRMS and SPMS. MCP1/CCL2 was found to be the most effective classifier between BMS and RRMS, while BMS was most effectively distinguished from SPMS by the combination of sCD40L and IFNγ levels. Conclusions: These differences may facilitate personalized precision medicine and aid in the discovery of new therapeutic targets for disease progression through the improvement of patient stratification.

The Effect of Interferon-Beta Therapy on T-Helper 17/miR-326 and T-Helper 1/miR-29b-3p Axis in Relapsing-Remitting Multiple Sclerosis Patients

2021 ◽  
pp. 1-9
Author(s):  
Leila Karimi ◽  
Nahid Eskandari ◽  
Vahid Shaygannejad
Keyword(s):  
Multiple Sclerosis ◽  
Plasma Levels ◽  
Th17 Cells ◽  
Interferon Beta ◽  
Enzyme Linked Immunosorbent Assay ◽  
T Helper ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Multiple Sclerosis Patients ◽  
Relapsing Remitting Multiple Sclerosis

<b><i>Background:</i></b> We aimed to evaluate the therapeutic effects of interferon-beta (IFN-β) on hsa-miR29b-3p and hsa-miR326 in isolated T-helper (Th)1 and Th17 cells expressed by relapsing-remitting multiple sclerosis (RRMS) patients before and after 1 year of treatment with IFN-β. <b><i>Methods:</i></b> The study was done on 19 RRMS patients pre- and posttreatment with IFN-β to evaluate the frequency of Th1 and Th17 cells by flow cytometry. The expression level of hsa-miR-29b-3p and hsa-miR-326 in isolated Th1 and Th17 cells was assessed by quantitative polymerase chain reaction. Enzyme-linked immunosorbent assay was also used to measure the plasma levels of I interferon -gamma and interleukin (IL)-17A. <b><i>Results:</i></b> Th17 cells and plasma levels of IL-17A decreased in RRMS patients after IFN-β therapy but hsa-miR-29b-3p and hsa-miR-326 expression had no significant change in treated RRMS patients versus baseline. <i>MxA</i> gene expression was significantly induced upon IFN-β therapy in patients with RRMS. <b><i>Conclusion:</i></b> IFN-β therapy is more effective on Th17 than Th1, but it does not reform altered expression of hsa-miR-326 and hsa-miR-29b-3p in Th17 and Th1, respectively.

Intravenous immunoglobulin in relapsing-remitting multiple sclerosis: A dose-finding trial

Neurology ◽  
2008 ◽  
Vol 71 (4) ◽  
pp. 265-271 ◽  
Author(s):  
F. Fazekas ◽  
F. D. Lublin ◽  
D. Li ◽  
M. S. Freedman ◽  
H. P. Hartung ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Intravenous Immunoglobulin ◽  
Dose Finding ◽  
Relapsing Remitting ◽  
Remitting Multiple Sclerosis ◽  
Relapsing Remitting Multiple Sclerosis
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