The role of Th17 cells in patients with relapsing-remitting multiple sclerosis: Interleukin-17A and interleukin-17F serum levels

Babaloo, Zohreh; Aliparasti, Mohammad Reza; Babaiea, Farhad; Almasi, Shohreh; Baradaran, Behzad; Farhoudi, Mehdi

doi:10.1016/j.imlet.2015.01.001

Cited by 73 publications

(50 citation statements)

References 30 publications

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“…In patients with MS, the serum levels of IL‐17 and IL‐17F were higher, and it has also been shown that high expression of IL‐17 correlates with MS severity (Babaloo et al, ). Neutralization of IL‐17 or IL‐17 deficiency rendered mice resistant to the induction of EAE (Babaloo et al, ). These studies indicate that Th17 cells play a key role in the pathogenesis of EAE.…”

Section: T Cell–based Immunotherapy In Msmentioning

confidence: 99%

Diversity of immune cell types in multiple sclerosis and its animal model: Pathological and therapeutic implications

Cheng

Sun

Xie

et al. 2017

J of Neuroscience Research

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Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system with an autoimmune attack on the components of the myelin sheath and axons. The etiology of the disease remains largely unknown, but it is commonly acknowledged that the development of MS probably results from the interaction of environmental factors in conjunction with a genetic predisposition. Current therapeutic approaches can only ameliorate the clinical symptoms or reduce the frequency of relapse in MS. Most drugs used in this disease broadly suppress the functions of immune effector cells, which can result in serious side effects. Thus, new therapeutic methods resulting in greater efficacy and lower toxicity are needed. Toward this end, cellbased therapies are of increasing interest in the treatment of MS. Several immunoregulatory cell types, including regulatory Tcells, regulatory B cells, M2 macrophages, tolerogenic dendritic cells, and stem cells, have been developed as novel therapeutic tools for the treatment of MS. In this Review, we summarize studies on the application of these cell populations for the treatment of MS and its animal model, experimental autoimmune encephalomyelitis, and call for further research on applications and mechanisms by which these cells act in the treatment of MS.

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Section: T Cell–based Immunotherapy In Msmentioning

confidence: 99%

Diversity of immune cell types in multiple sclerosis and its animal model: Pathological and therapeutic implications

Cheng

Sun

Xie

et al. 2017

J of Neuroscience Research

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“…Th17 cells represent a proinflammatory subset, and, in excess, contribute to autoimmunity and tissue damage; Treg cells play a major role in controlling autoimmunity, and, when deficient, contribute to these diseases [6]. Recent studies have shown that Th17 and Treg cells and their related cytokines (interleukin [IL]-17, IL-6, IL-23, IL-21, transforming growth factor [TGF]-β1, and IL-10) are linked to the progression of both multiple sclerosis (MS) and NMOSD [7-11]. It has been postulated that Th17 cells play a more relevant role in the initial phases of experimental autoimmune encephalomyelitis and MS [12].…”

Section: Introductionmentioning

confidence: 99%

Cytokines and Tissue Damage Biomarkers in First-Onset Neuromyelitis Optica Spectrum Disorders: Significance of Interleukin-6

Wei

Chang

et al. 2018

Neuroimmunomodulation

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Objective: We investigated the contribution of several cytokines in the pathogenesis of first-onset neuromyelitis optica spectrum disorder (NMOSD) and determined the differences between aquaporin 4 immunoglobulin G (AQP4-IgG)-positive and AQP4-IgG-negative subtypes. Methods: We enrolled 18 NMOSD (10 AQP4-IgG-positive and 8 AQP4-IgG-negative) and 8 multiple sclerosis (MS) patients, whose serum and cerebrospinal fluid (CSF) samples were collected during the acute phase of the first onset before immunotherapy. Fifteen patients with other noninflammatory neurological diseases (OND) were also included. The serum and CSF levels of interleukin (IL)-6, IL-10, IL-17, IL-21, IL-23, transforming growth factor (TGF)-β1 and the CSF levels of 3 biomarkers of axonal loss and astrocytic damage were measured using the human cytokine multiplex assay or ELISA. Results: Serum levels of IL-10 and TGF-β1 and CSF levels of IL-6, IL-10, and TGF-β1 were significantly increased in first-onset NMOSD compared to in OND patients. In a subgroup analysis, the CSF levels of IL-6, neurofilament light protein (NFL), S100B, and glial fibrillary acidic protein (GFAP) were significantly more elevated in the AQP4-IgG-positive patients than in the AQP4-IgG-negative NMOSD patients. Correlations were found between the CSF cytokines and tissue damage biomarkers and the clinical findings in NMOSD patients. Notably, the CSF IL-6 level had the strongest correlation with the tissue damage biomarkers and it also correlated with CSF white blood cell (WBC) count. Conclusions: IL-6 plays a role in the pathogenetic process of NMOSD, especially in the AQP4-IgG-positive subtype. Distinct pathogenesis exists between AQP4-IgG-positive and AQP4-IgG-negative NMOSD in the initial phase of the disease.

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“…Besides the described protective properties of T H 17 cells, this cell type is apparently also associated with autoimmune diseases, chronic inflammatory conditions, and carcinogenesis. Multiple sclerosis, rheumatoid arthritis, IBD, and psoriasis are amongst the diseases with a strong T H 17 cell involvement [75,76,77,78]. Additionally, as discussed above, uncontrolled IL-22, IL-17, and TNF-α level can promote carcinogenesis.…”

Section: Control Of Th17 Cellsmentioning

confidence: 99%

Regulation of TH17 Cells and Associated Cytokines in Wound Healing, Tissue Regeneration, and Carcinogenesis

Brockmann

Giannou

Gagliani

et al. 2017

IJMS

124

115

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Wound healing is a crucial process which protects our body against permanent damage and invasive infectious agents. Upon tissue damage, inflammation is an early event which is orchestrated by a multitude of innate and adaptive immune cell subsets including TH17 cells. TH17 cells and TH17 cell associated cytokines can impact wound healing positively by clearing pathogens and modulating mucosal surfaces and epithelial cells. Injury of the gut mucosa can cause fast expansion of TH17 cells and their induction from naïve T cells through Interleukin (IL)-6, TGF-β, and IL-1β signaling. TH17 cells produce various cytokines, such as tumor necrosis factor (TNF)-α, IL-17, and IL-22, which can promote cell survival and proliferation and thus tissue regeneration in several organs including the skin, the intestine, and the liver. However, TH17 cells are also potentially pathogenic if not tightly controlled. Failure of these control mechanisms can result in chronic inflammatory conditions, such as Inflammatory Bowel Disease (IBD), and can ultimately promote carcinogenesis. Therefore, there are several mechanisms which control TH17 cells. One control mechanism is the regulation of TH17 cells via regulatory T cells and IL-10. This mechanism is especially important in the intestine to terminate immune responses and maintain homeostasis. Furthermore, TH17 cells have the potential to convert from a pro-inflammatory phenotype to an anti-inflammatory phenotype by changing their cytokine profile and acquiring IL-10 production, thereby limiting their own pathological potential. Finally, IL-22, a signature cytokine of TH17 cells, can be controlled by an endogenous soluble inhibitory receptor, Interleukin 22 binding protein (IL-22BP). During tissue injury, the production of IL-22 by TH17 cells is upregulated in order to promote tissue regeneration. To limit the regenerative program, which could promote carcinogenesis, IL-22BP is upregulated during the later phase of regeneration in order to terminate the effects of IL-22. This delicate balance secures the beneficial effects of IL-22 and prevents its potential pathogenicity. An important future goal is to understand the precise mechanisms underlying the regulation of TH17 cells during inflammation, wound healing, and carcinogenesis in order to design targeted therapies for a variety of diseases including infections, cancer, and immune mediated inflammatory disease.

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The role of Th17 cells in patients with relapsing-remitting multiple sclerosis: Interleukin-17A and interleukin-17F serum levels

Cited by 73 publications

References 30 publications

Diversity of immune cell types in multiple sclerosis and its animal model: Pathological and therapeutic implications

Diversity of immune cell types in multiple sclerosis and its animal model: Pathological and therapeutic implications

Cytokines and Tissue Damage Biomarkers in First-Onset Neuromyelitis Optica Spectrum Disorders: Significance of Interleukin-6

Regulation of TH17 Cells and Associated Cytokines in Wound Healing, Tissue Regeneration, and Carcinogenesis

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