β-defensin-3 negatively regulates TLR4–HMGB1 axis mediated HLA-G expression in IL-1β treated glioma cells

Gupta, Piyushi; Ghosh, Sadashib; Nagarajan, Ashwat; Mehta, Veer Singh; Sen, Ellora

doi:10.1016/j.cellsig.2012.12.001

Cited by 32 publications

(25 citation statements)

References 37 publications

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“…HMGB1 is a non-histone chromosome-binding protein expressed in eukaryotic cells. It was first found to express in the brain and extensively express in heart, liver, spleen, lung, and kidney tissues (Gupta, Ghosh, & Nagarajan, 2013;Wang, Ward, & Sama, 2014). The extracellular HMGB1 is first found in the brain tissue, which is mainly related to immunoregulation.…”

Section: Discussionmentioning

confidence: 99%

High expression of the HMGB1–TLR4 axis and its downstream signaling factors in patients with Parkinson's disease and the relationship of pathological staging

Yang

Han

et al. 2018

Brain and Behavior

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ObjectiveTo detect the expression of high‐mobility group box protein 1 (HMGB1) and toll‐like receptor 4 (TLR4) and their downstream signaling factors—myeloid differentiation factor 88 (MyD88), nuclear factor kappa B (NF‐κB), and tumor necrosis factor alpha (TNF‐α)—in the sera of patients with Parkinson's disease (PD) in order to evaluate the relationship of the HMGB1–TLR4 axis with PD development and progression.MethodsThe serum HMGB1 and TLR4 protein levels of 120 patients with PD and 100 healthy volunteers were measured using double‐antibody sandwich ELISA, and their correlations with PD staging, disease duration, drug treatment effectiveness, and clinical classification were analyzed. In addition, their correlations with the key downstream factors of the HMGB1–TLR4 axis (MyD88, NF‐κB, and TNF‐α) were analyzed.ResultsHMGB1 and TLR4 expressions were higher in the peripheral blood of patients with PD than in healthy volunteers. PD patients with poor drug treatment outcomes had significantly higher HMGB1 and TLR4 expressions than PD patients with stable drug treatment outcomes. Higher HMGB1 and TLR4 expressions were found in patients at higher PD stages, and patients with >4‐year disease duration had significantly higher HMGB1 and TLR4 expressions than patients with <4‐year disease duration. No significant difference in HMGB1 and TLR4 expressions was found among patients with tremor‐dominant, akinetic‐rigid, and mixed subtypes of PD. NF‐κB and TNF‐α expressions were positively correlated with high expression of the HMGB1–TLR4 axis.ConclusionHigh expression of the HMGB1–TLR4 axis is closely associated with PD development, progression, drug treatment effectiveness, staging, and disease duration and has great significance for PD diagnosis and treatment.

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Section: Discussionmentioning

confidence: 99%

High expression of the HMGB1–TLR4 axis and its downstream signaling factors in patients with Parkinson's disease and the relationship of pathological staging

Yang

Han

et al. 2018

Brain and Behavior

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“…Previous reports indicate a role for Hmgb1 in the proliferation and migration of endothelial cells in vitro (30) and in vascular bed remodeling in models of ischemia-reperfusion injury (40) (41). Little is known about the relationship between Hmgb1 and Hif1a (42)(43)(44). Further studies are required to better delineate the interaction, verifying in particular whether MAPK is involved (45)(46)(47) and whether oxygen sensing in endothelial cells or stromal cells is modified in the absence of leukocyte Hmgb1.…”

Section: Discussionmentioning

confidence: 99%

Leukocyte HMGB1 Is Required for Vessel Remodeling in Regenerating Muscles

Campana

Santarella

Esposito

et al. 2014

The Journal of Immunology

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Signals of tissue necrosis, damage-associated molecular patterns (DAMPs), cause inflammation. Leukocytes migrating into injured tissues tonically release DAMPs, including the high mobility group box 1 protein (HMGB1). In the absence of suitable models, the relative role of DAMPs released because of necrosis or leukocyte activation has not, so far, been dissected. We have generated a mouse model lacking Hmgb1 in the hematopoietic system and studied the response to acute sterile injury of the skeletal muscle. Regenerating fibers are significantly less numerous at earlier time points and smaller at the end of the process. Leukocyte Hmgb1 licenses the skeletal muscle to react to hypoxia, to express angiopoietin-2, and to initiate angiogenesis in response to injury. Vascularization of the regenerating tissue is selectively jeopardized in the absence of leukocyte Hmgb1, revealing that it controls the nutrient and oxygen supply to the regenerating tissue. Altogether, our results reveal a novel nonredundant role for leukocyte Hmgb1 in the repair of injured skeletal muscle.

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“…Indeed, TNF- α has been shown to induce a moderate increase in steady-state levels of HLA-G mRNA in human trophoblast cell lines [98]. IL-1 β increases the expression of HLA-G and Toll-like receptor 4 (TLR4) in an HIF-1 α -dependent manner [104]. …”

Section: Mechanisms Of Hla-g Modulation During Infectionmentioning

confidence: 99%

Immunomodulatory Properties of HLA-G in Infectious Diseases

Amiot

Samson

2014

Journal of Immunology Research

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HLA-G is a nonclassical major histocompatibility complex molecule first described at the maternal-fetal interface, on extravillous cytotrophoblasts. Its expression is restricted to some tissues in normal conditions but increases strongly in pathological conditions. The expression of this molecule has been studied in detail in cancers and is now also beginning to be described in infectious diseases. The relevance of studies on HLA-G expression lies in the well known inhibitory effect of this molecule on all cell types involved in innate and adaptive immunity, favoring escape from immune control. In this review, we summarize the features of HLA-G expression by type of infections (i.e, bacterial, viral, or parasitic) detailing the state of knowledge for each pathogenic agent. The polymorphism, the interference of viral proteins with HLA-G intracellular trafficking, and various cytokines have been described to modulate HLA-G expression during infections. We also discuss the cellular source of HLA-G, according to the type of infection and the potential role of HLA-G. New therapeutic approaches based on synthetic HLA-G-derived proteins or antibodies are emerging in mouse models of cancer or transplantation, and these new therapeutic tools may eventually prove useful for the treatment of infectious diseases.

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β-defensin-3 negatively regulates TLR4–HMGB1 axis mediated HLA-G expression in IL-1β treated glioma cells

Cited by 32 publications

References 37 publications

High expression of the HMGB1–TLR4 axis and its downstream signaling factors in patients with Parkinson's disease and the relationship of pathological staging

High expression of the HMGB1–TLR4 axis and its downstream signaling factors in patients with Parkinson's disease and the relationship of pathological staging

Leukocyte HMGB1 Is Required for Vessel Remodeling in Regenerating Muscles

Immunomodulatory Properties of HLA-G in Infectious Diseases

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