Toll like receptors: a new hope on the horizon to treat multiple sclerosis

Gooshe, Maziar; Aleyasin, Ali Reza; Abdolghaffari, Amir Hossein; Rezaei, Nima

doi:10.1586/1744666x.2014.953061

Cited by 12 publications

(5 citation statements)

References 19 publications

(21 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since MyD88 is essential for most TLRs (except TLR3 and part of TLR4), inhibition of MyD88 is expected to have a therapeutic effect on MS. For example, the short form of MyD88 (sMyD88) can inhibit TLR-MyD88 signaling by preventing IRAK1 phosphorylation. BB-loop decoy peptides inhibit the TLR-MyD88 signaling pathway by interfering with the MyD88 TIR domain or the full-length MyD88 (Gooshe et al, 2014b).…”

Section: Therapy Of Ms Via Targeting the Tlr-myd88 Pathwaymentioning

confidence: 99%

Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis

Chen

Chu

et al. 2020

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Multiple sclerosis (MS) is a neuro-autoimmune and neurodegenerative disorder leading to chronic inflammation, demyelination, axonal, and neuronal loss in the central nervous system (CNS). Despite intense research efforts, the pathogenesis of MS still remains unclear. Toll-like receptors (TLRs) are a family of type I transmembrane receptors that play a crucial role in the innate immune response. Myeloid differentiation factor 88 (MyD88) is the adaptor of major TLRs. It has been widely considered that the TLR-MyD88 signaling pathway plays an important role in the occurrence and development of autoimmune disease. Data have revealed that the TLR-MyD88 signaling may be involved in the pathogenesis of MS and experimental autoimmune encephalomyelitis (EAE), an animal model for MS, by regulating the antigen presentation of dendritic cells, the integrity of blood-brain barrier (BBB), and the activation of T cells and B cells. Here, we summarize the role of TLRs and MyD88 in MS and discuss the possible therapies that are based on these molecules.

show abstract

Section: Therapy Of Ms Via Targeting the Tlr-myd88 Pathwaymentioning

confidence: 99%

Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis

Chen

Chu

et al. 2020

Front. Mol. Neurosci.

View full text Add to dashboard Cite

show abstract

“…These are expressed in various immune and non-immune cells and most CNS cells like microglia, astrocyte, neuron and oligodendrocyte. Activation of subsequent pathways with TLRs could trigger the production of proin ammatory cytokines like IL-1, IL-12, and TNFα and induce pro-in ammatory pathways, such as NFκB and MAPK [ 10,11]. Different stimuli activate the NFB pathway, which then translocate to nuclei.…”

Section: Pathogenesismentioning

confidence: 99%

Platelets-derived vesicles: innovative subcellular platforms for management of multiple sclerosis

Mehdi-Alamdarlou

Ahmadi

Shahbazi

et al. 2022

Preprint

View full text Add to dashboard Cite

Multiple sclerosis (MS) is a progressive inflammatory autoimmune disease that involves young individuals. The drug delivery systems now are available for this disease have chronic and non-targeted effects in the patients, and because of the presence of BBB, their concentration in the CNS is low. Because of this flaw, it is critical to use innovative active targeted drug delivery methods. Platelets are blood cells that circulate freely and play an important role in blood hemostasis. In this review, we emphasize the various roles of activated platelets in the inflammatory condition to recruit other cells to the injured area and limit the inflammation. Besides, the activated platelets in the different stages of the MS disease play a significant role for limiting the progression of inflammation in the peripheral area and CNS. This evidence indicates that platelet-based drug delivery system can be an efficient candidate for drug targeting to the CNS and limiting the inflammation in the peripheral and central areas for MS therapy.

show abstract

“…Indeed, TLRs activation lead to the recruitment of adaptor proteins within the cytosol, that culminates in signal transduction resulting in the transcription of genes involved in chronic inflammation [ 72 , 73 ]. TLRs were initially identified as receptors important only in host defences, but it is now clear that the TLRs, for example TLR2 and TLR4, are crucial in autoimmunity development [ 74 , 75 , 76 ], as demonstrated in RA [ 74 ], SLE [ 77 ], multiple sclerosis [ 78 ], and inflammatory bowel diseases [ 79 ]. Studies comparing mice and humans revealed that numerous types of epithelial cells express TLRs, supporting the hypothesis that the epithelium represents the first line of defence of the innate immune system [ 80 , 81 ].…”

Section: Toll-like Receptor-mediated Nf-κb Activation In Pssmentioning

confidence: 99%

Understanding the Complexity of Sjögren’s Syndrome: Remarkable Progress in Elucidating NF-κB Mechanisms

Sisto

Ribatti

Lisi

2020

JCM

View full text Add to dashboard Cite

Sjögren’s syndrome (SS) is a systemic autoimmune inflammatory disease with a poorly defined aetiology, which targets exocrine glands (particularly salivary and lachrymal glands), affecting the secretory function. Patients suffering from SS exhibit persistent xerostomia and keratoconjunctivitis sicca. It is now widely acknowledged that a chronic grade of inflammation plays a central role in the initiation, progression, and development of SS. Consistent with its key role in organizing inflammatory responses, numerous recent studies have shown involvement of the transcription factor nuclear factor κ (kappa)-light-chain-enhancer of activated B cells (NF-κB) in the development of this disease. Therefore, chronic inflammation is considered as a critical factor in the disease aetiology, offering hope for the development of new drugs for treatment. The purpose of this review is to describe the current knowledge about the NF-κB-mediated molecular events implicated in the pathogenesis of SS.

show abstract

Toll like receptors: a new hope on the horizon to treat multiple sclerosis

Cited by 12 publications

References 19 publications

Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis

Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis

Platelets-derived vesicles: innovative subcellular platforms for management of multiple sclerosis

Understanding the Complexity of Sjögren’s Syndrome: Remarkable Progress in Elucidating NF-κB Mechanisms

Contact Info

Product

Resources

About