Elevated plasma high-mobility group box 1 protein is a potential marker for neuromyelitis optica

Wang, K.-C.; Tsai, Ching Piao; Lee, C.-L.; Chen, S.-Y.; Chin, Li Te; Chen, S.-J.

doi:10.1016/j.neuroscience.2012.08.041

Cited by 28 publications

(14 citation statements)

References 41 publications

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“…Up-regulated HMGB1 levels have been systemically detected in inflammatory autoimmune-mediated diseases in animal models and patients, indicating that HMGB1 has important roles in these diseases. Extracellular HMGB1 was also detected in the target organs in T cell-mediated, organ-specific autoimmune diseases, for example, in the aqueous humor of EAU induced by immunization of IRBP and CFA in Lewis rats [41] and in CSF of patients with NMO and MS [42][43][44]. In the former, increased HMGB1 seems to be associated with infiltrating inflammatory cells, as HMGB1 in the AqH was increased significantly at the peak of intraocular inflammation (Day 14 postimmunization) [41]; in the latter, CSF HMGB1 levels were high during the relapse phase of NMO and MS, especially NMO [42].…”

Section: Discussionmentioning

confidence: 99%

HMGB1 is an early and critical mediator in an animal model of uveitis induced by IRBP-specific T cells

Jiang

Sun

Yang

et al. 2013

Journal of Leukocyte Biology

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It is largely unknown how invading autoreactive T cells initiate the pathogenic process inside the diseased organ in organ-specific autoimmune disease. In this study, we used a chronic uveitis disease model in mice--EAU--induced by adoptive transfer of uveitogenic IRBP-specific T cells and showed that HMGB1, an important endogenous molecule that serves as a danger signal, was released rapidly from retinal cells into the ECM and intraocular fluid in response to IRBP-specific T cell transfer. HMGB1 release required direct cell-cell contact between retinal cells and IRBP-specific T cells and was an active secretion from intact retinal cells. Administration of HMGB1 antagonists inhibited severity of EAU significantly via mechanisms that include inhibition of IRBP-specific T cell proliferation and their IFN-γ and IL-17 production. The inflammatory effects of HMGB1 may signal the TLR/MyD88 pathway, as MyD88(-/-) mice had a high level of HMGB1 in the eye but did not develop EAU after IRBP-specific T cell transfer. Our study demonstrates that HMGB1 is an early and critical mediator of ocular inflammation initiated by autoreactive T cell invasion.

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Section: Discussionmentioning

confidence: 99%

HMGB1 is an early and critical mediator in an animal model of uveitis induced by IRBP-specific T cells

Jiang

Sun

Yang

et al. 2013

Journal of Leukocyte Biology

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“…This disease can lead to loss of vision, muscle strength, and coordination, sensory impairment, and paraplegia or even tetraplegia. Serum and cerebrospinal fluid HMGB1 levels are significantly greater in patients with neuromyelitis optica, suggesting that HMGB1 might be a diagnostic marker for neuromyelitis optica in the early stage (Uzawa et al, 2013a; Wang et al, 2013c; Wang et al, 2012a). …”

Section: Hmgb1 and Diseasementioning

confidence: 99%

HMGB1 in health and disease

Kang

Chen

Zhang

et al. 2014

Molecular Aspects of Medicine

822

828

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Complex genetic and physiological variations as well as environmental factors that drive emergence of chromosomal instability, development of unscheduled cell death, skewed differentiation, and altered metabolism are central to the pathogenesis of human diseases and disorders. Understanding the molecular bases for these processes is important for the development of new diagnostic biomarkers, and for identifying new therapeutic targets. In 1973, a group of non-histone nuclear proteins with high electrophoretic mobility was discovered and termed High-Mobility Group (HMG) proteins. The HMG proteins include three superfamilies termed HMGB, HMGN, and HMGA. High-mobility group box 1 (HMGB1), the most abundant and well-studied HMG protein, senses and coordinates the cellular stress response and plays a critical role not only inside of the cell as a DNA chaperone, chromosome guardian, autophagy sustainer, and protector from apoptotic cell death, but also outside the cell as the prototypic damage associated molecular pattern molecule (DAMP). This DAMP, in conjunction with other factors, thus has cytokine, chemokine, and growth factor activity, orchestrating the inflammatory and immune response. All of these characteristics make HMGB1 a critical molecular target in multiple human diseases including infectious diseases, ischemia, immune disorders, neurodegenerative diseases, metabolic disorders, and cancer. Indeed, a number of emergent strategies have been used to inhibit HMGB1 expression, release, and activity in vitro and in vivo. These include antibodies, peptide inhbitiors, RNAi, anti-coagulants, endogenous hormones, various chemical compounds, HMGB1-receptor and signaling pathway inhibition, artificial DNAs, physical strategies including vagus nerve stimulation and other surgical approaches. Future work further investigating the details of HMGB1 localizationtion, structure, post-translational modification, and identifccation of additional partners will undoubtedly uncover additional secrets regarding HMGB1’s multiple functions.

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“…The findings were statistically significant and demonstrated that GFAP levels in patients with ON related to NMO are higher than those in MS suggesting that it can be a good biomarker in atypical presentations [53]. One single study suggested that high-mobility group box 1 protein (HMGB1) in serum can be used as an early diagnostic tool in NMO, making its distinction from MS possible [54].…”

Section: Sarcoidosismentioning

confidence: 99%

Neuromyelitis optica spectrum disorders associated with other autoimmune diseases

Freitas

Guimarães

2014

Rheumatol Int

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Neuromyelitis optica (NMO) is an inflammatory demyelinating autoimmune disease with severe, tremendously incapacitating, consequences in the patient's health and wellbeing. Until 2004, NMO was considered a restricted type of multiple sclerosis but in the same year an auto-antibody reacting against aquaporin-4 (NMO-IgG) was found to be related with NMO and it was considered the main etiologic agent of this disease. Its detection is very sensitive and specific allowing an early diagnosis and a better treatment and prognosis. With this tool, a spectrum of diseases including other autoimmune diseases was found to have NMO-IgG antibodies and a new classification named NMO spectrum disorders was created. In this review, we sum up the developments in this field associated with other autoimmune diseases. We approach the latest discoveries in the diagnosis like the new biomarkers that will possibly be used in the close future or the developments in the neuroimaging techniques. We reviewed the literature and synthesized case reports of NMO patients with concurrent autoimmune diseases and the information from useful larger studies. Finally, we summarize the commonly used treatments in NMO and we try to specify the best treatment for NMO with simultaneous autoimmune disease. This review updates the information about this issue and raises the awareness of rheumatologists for these severe diseases.

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Elevated plasma high-mobility group box 1 protein is a potential marker for neuromyelitis optica

Cited by 28 publications

References 41 publications

HMGB1 is an early and critical mediator in an animal model of uveitis induced by IRBP-specific T cells

HMGB1 is an early and critical mediator in an animal model of uveitis induced by IRBP-specific T cells

HMGB1 in health and disease

Neuromyelitis optica spectrum disorders associated with other autoimmune diseases

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