TLR/MyD88-mediated Innate Immunity in Intestinal Graft-versus-Host Disease

Lee, Youngkwan; Kang, Myung-Soo; Choi, Eun Young

doi:10.4110/in.2017.17.3.144

Cited by 25 publications

(19 citation statements)

References 70 publications

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“…The activation of MyD88 leads to the activation of NF-κB, MAPKs, and activator protein 1 (AP-1; Deguine and Barton, 2014). The activation of these signaling pathways results in the production of pro-inflammatory cytokines such as IL-1, IL-6, and INF-α by activating downstream molecules (Lee et al, 2017). In neurons, IL-1β activation depends on two signaling pathways.…”

Section: Myd88mentioning

confidence: 99%

Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis

Chen

Chu

et al. 2020

Front. Mol. Neurosci.

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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.

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Section: Myd88mentioning

confidence: 99%

Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis

Chen

Chu

et al. 2020

Front. Mol. Neurosci.

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“…Priming is initiated by the interaction between extracellular pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs), the pathogen-associated molecular patterns (PAMPs), and the danger-associated molecular patterns (DAMPs) [1,2]. This interaction, in turn, induces the signal transduction cascades of intracellular molecules in the inflammatory signaling pathways, such as nuclear factor-kappa B (NF-κB), activator protein-1 (AP-1), and interferon (IFN) regulatory factors (IRFs), resulting in the production of inflammatory molecules, such as nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) and pro-inflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin (IL)-1B, IL-6, and IFNs [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Caspase-11 Non-Canonical Inflammasome: Emerging Activator and Regulator of Infection-Mediated Inflammatory Responses

2020

IJMS

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Inflammation is a body's protective mechanism to eliminate invading pathogens and cellular damaging signals. The inflammatory response consists of two main consecutive steps-a priming step preparing the inflammatory responses and a triggering step boosting the inflammatory responses. The main feature of the triggering step is the activation of the inflammasome, an intracellular multiprotein complex facilitating the inflammatory responses. The regulatory roles of 'canonical' inflammasomes in the inflammatory responses and diseases have been largely investigated, so far. New types of inflammasomes have been recently discovered and named as 'non-canonical' inflammasomes since their roles to induce inflammatory responses are similar to those of canonical inflammasomes, however, the stimulating ligands and the underlying mechanisms are different. Therefore, a growing number of studies have actively investigated the novel roles of non-canonical inflammasomes in inflammatory responses and diseases. This review summarizes and discusses the recent studies exploring the regulatory roles of caspase-11 non-canonical inflammasome during the inflammatory responses and provides insight into the development of novel therapeutics for infectious and inflammatory diseases by targeting caspase-11 non-canonical inflammasome.

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“…We have seen over many years that innate immune defense systems mounted at epithelial surfaces perform multiple and often non-immune roles. The toll-like receptor system is a classic example that has transformed our perception about the origins of innate immunity and its roles in insect development ( 1 , 2 ), antimicrobial defense ( 3 ) and in the pathogenesis of some inflammatory conditions ( 4 – 6 ). The complement system Figure 1 has been known about for longer ( 7 ), but the diversity of function and, in particular, its role at the interface between innate and adaptive immunity can now be re-visited as a typical model for innate immune function as well as a therapeutic target in a growing number of medical disorders.…”

Section: Introductionmentioning

confidence: 99%

Collectin-11 (CL-11) Is a Major Sentinel at Epithelial Surfaces and Key Pattern Recognition Molecule in Complement-Mediated Ischaemic Injury

et al. 2018

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The complement system is a dynamic subset of the innate immune system, playing roles in host defense, clearance of immune complexes and cell debris, and priming the adaptive immune response. Over the last 40 years our understanding of the complement system has evolved from identifying its presence and recognizing its role in the blood to now focusing on understanding the role of local complement synthesis in health and disease. In particular, the local synthesis of complement was found to have an involvement in mediating ischaemic injury, including following transplantation. Recent work on elucidating the triggers of local complement synthesis and activation in renal tissue have led to the finding that Collectin-11 (CL-11) engages with L-fucose at the site of ischaemic stress, namely at the surface of the proximal tubular epithelial cells. What remains unknown is the precise structure of the damage-associated ligand that participates in CL-11 binding and subsequent complement activation. In this article, we will discuss our hypothesis regarding the role of CL-11 as an integral tissue-based pattern recognition molecule which we postulate has a significant contributory role in complement-mediated ischaemic injury.

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TLR/MyD88-mediated Innate Immunity in Intestinal Graft-versus-Host Disease

Cited by 25 publications

References 70 publications

Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis

Inflammatory Role of TLR-MyD88 Signaling in Multiple Sclerosis

Caspase-11 Non-Canonical Inflammasome: Emerging Activator and Regulator of Infection-Mediated Inflammatory Responses

Collectin-11 (CL-11) Is a Major Sentinel at Epithelial Surfaces and Key Pattern Recognition Molecule in Complement-Mediated Ischaemic Injury

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