Regulatory T cell number in multiple sclerosis patients: A meta-analysis

Noori-Zadeh, Ali; Mesbah‐Namin, Seyed Alireza; Bistoon-beigloo, Sara; Bakhtiyari, Salar; Abbaszadeh, Hojjat-Allah; Darabi, Shahram; Rajabibazl, Masoumeh; Abdanipour, Alireza

doi:10.1016/j.msard.2015.11.004

Cited by 41 publications

(21 citation statements)

References 25 publications

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“…Abnormal quantity or function of Tregs leads to immune‐related diseases. For example, in multiple sclerosis (MS) or myasthenia gravis (MG), although significant differences in the number of circulating Tregs relative to healthy controls are not frequently observed, Tregs from these patients are found to have a lower suppressive capacity . Many MS patients have decreased FoxP3 expression in Tregs .…”

Section: Treg and Th17 Cells: Features Functions And Their Interplaysmentioning

confidence: 99%

Regulatory T cells and T helper 17 cells in viral infection

et al. 2020

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CD4 + T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4 + T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection. How to cite this article: Wan Z, Zhou Z, Liu Y, et al. Regulatory T cells and T helper 17 cells in viral infection. Scand J Immunol. 2020;91:e12873.

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Section: Treg and Th17 Cells: Features Functions And Their Interplaysmentioning

confidence: 99%

Regulatory T cells and T helper 17 cells in viral infection

et al. 2020

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“…Tregs regulate immune response in the periphery predominantly by suppressing Teff cells. Although significant differences in the number of circulating Tregs in MS or MG patients relative to healthy controls are not frequently reported, Tregs from these patients are reported to have lower suppressive capabilities [1, 13, 60, 61]. This suggests that functional deficits in Tregs may contribute to the pathogenesis of MS and MG. For example, defects in Treg suppressor molecules have been linked to MS, such as reduced IL-10 production and genetic variations in CD25 [27, 55].…”

Section: Main Textmentioning

confidence: 99%

Regulatory T cells in multiple sclerosis and myasthenia gravis

Danikowski

Jayaraman

Prabhakar

2017

J Neuroinflammation

262

171

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Multiple sclerosis (MS) is a chronic debilitating disease of the central nervous system primarily mediated by T lymphocytes with specificity to neuronal antigens in genetically susceptible individuals. On the other hand, myasthenia gravis (MG) primarily involves destruction of the neuromuscular junction by antibodies specific to the acetylcholine receptor. Both autoimmune diseases are thought to result from loss of self-tolerance, which allows for the development and function of autoreactive lymphocytes. Although the mechanisms underlying compromised self-tolerance in these and other autoimmune diseases have not been fully elucidated, one possibility is numerical, functional, and/or migratory deficits in T regulatory cells (Tregs). Tregs are thought to play a critical role in the maintenance of peripheral immune tolerance. It is believed that Tregs function by suppressing the effector CD4+ T cell subsets that mediate autoimmune responses. Dysregulation of suppressive and migratory markers on Tregs have been linked to the pathogenesis of both MS and MG. For example, genetic abnormalities have been found in Treg suppressive markers CTLA-4 and CD25, while others have shown a decreased expression of FoxP3 and IL-10. Furthermore, elevated levels of pro-inflammatory cytokines such as IL-6, IL-17, and IFN-γ secreted by T effectors have been noted in MS and MG patients. This review provides several strategies of treatment which have been shown to be effective or are proposed as potential therapies to restore the function of various Treg subsets including Tr1, iTr35, nTregs, and iTregs. Strategies focusing on enhancing the Treg function find importance in cytokines TGF-β, IDO, interleukins 10, 27, and 35, and ligands Jagged-1 and OX40L. Likewise, strategies which affect Treg migration involve chemokines CCL17 and CXCL11. In pre-clinical animal models of experimental autoimmune encephalomyelitis (EAE) and experimental autoimmune myasthenia gravis (EAMG), several strategies have been shown to ameliorate the disease and thus appear promising for treating patients with MS or MG.

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“…In recent years, cell therapy (1,2) and gene therapy have gained a considerable attention as a solution for disease treatments (3,4). BMSCs are widely used as an available source for cell therapy and tissue engineering (5).…”

Section: Introductionmentioning

confidence: 99%