Abstract：
BACKGROUND:Antibodies with specificity for myelin oligodendrocyte glycoprotein (MOG) are implicated in multiple sclerosis and related diseases. The pathogenic importance of anti-MOG antibody in primary demyelinating pathology remains poorly characterized. OBJECTIVE:The objective of this study is to investigate whether administration of anti-MOG antibody would be sufficient for demyelination and to determine if type I interferon (IFN) signaling plays a similar role in anti-MOG antibody-mediated pathology, as has been shown for neuromyelitis optica-like pathology. METHODS:Purified IgG2a monoclonal anti-MOG antibody and mouse complement were stereotactically injected into the corpus callosum of wild-type and type I IFN receptor deficient mice (IFNAR1-KO) with and without pre-established experimental autoimmune encephalomyelitis (EAE). RESULTS:Anti-MOG induced complement-dependent demyelination in the corpus callosum of wild-type mice and did not occur in mice that received control IgG2a. Deposition of activated complement coincided with demyelination, and this was significantly reduced in IFNAR1-KO mice. Co-injection of anti-MOG and complement at onset of symptoms of EAE induced similar levels of callosal demyelination in wild-type and IFNAR1-KO mice. CONCLUSIONS:Anti-MOG antibody and complement was sufficient to induce callosal demyelination, and pathology was dependent on type I IFN. Induction of EAE in IFNAR1-KO mice overcame the dependence on type I IFN for anti-MOG and complement-mediated demyelination.
journal_name
J Neuroinflammationjournal_title
Journal of neuroinflammationauthors
Berg CT,Khorooshi R,Asgari N,Owens Tdoi
10.1186/s12974-017-0899-1subject
Has Abstractpub_date
2017-06-24 00:00:00pages
127issue
1issn
1742-2094pii
10.1186/s12974-017-0899-1journal_volume
14pub_type
杂志文章abstract：BACKGROUND:Local and systemic inflammatory responses are initiated early after traumatic brain injury (TBI), and may play a key role in the secondary injury processes resulting in neuronal loss and neurological deficits. However, the mechanisms responsible for the rapid expansion of neuroinflammation and its long-term ...
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abstract：BACKGROUND:The chemokine interleukin-8 (IL-8) and its receptor CXCR2 contribute to chemotactic responses in Alzheimer's disease (AD); however, properties of the ligand and receptor have not been characterized in animal models of disease. The primary aim of our study was to examine effects of pharmacological antagonism ...
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journal_title：Journal of neuroinflammation
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doi：10.1186/s12974-016-0539-1
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章,评审
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
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abstract：:Human immunodeficiency virus type 1 (HIV) continues to be one of the most prevalent global health afflictions to date. The advent and introduction of combined antiretroviral therapy (cART) has made a significant impact on the course of infection. However, as patients are living longer, many HIV-associated illnesses ar...
journal_title：Journal of neuroinflammation
pub_type： 杂志文章,评审
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journal_title：Journal of neuroinflammation
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journal_title：Journal of neuroinflammation
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
doi：10.1186/s12974-016-0787-0
更新日期：2017-01-13 00:00:00
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章,评审
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
doi：10.1186/1742-2094-7-29
更新日期：2010-05-04 00:00:00
abstract：BACKGROUND:Progression of neurodegenerative diseases occurs when microglia, upon persistent activation, perpetuate a cycle of damage in the central nervous system. Use of mesenchymal stem cells (MSC) has been suggested as an approach to manage microglia activation based on their immunomodulatory functions. In the prese...
journal_title：Journal of neuroinflammation
pub_type： 杂志文章
doi：10.1186/s12974-014-0149-8
更新日期：2014-09-03 00:00:00
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
doi：10.1186/1742-2094-8-142
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journal_title：Journal of neuroinflammation
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更新日期：2019-10-28 00:00:00
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
doi：10.1186/s12974-015-0453-y
更新日期：2015-12-30 00:00:00
abstract：BACKGROUND:HIV-associated neuroinflammation is believed to be a major contributing factor in the development of HIV-associated neurocognitive disorders (HAND). In this study, we used micropositron emission tomography (PET) imaging to quantify neuroinflammation in HIV-1 transgenic rat (Tg), a small animal model of HIV, ...
journal_title：Journal of neuroinflammation
pub_type： 杂志文章
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journal_title：Journal of neuroinflammation
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journal_title：Journal of neuroinflammation
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journal_title：Journal of neuroinflammation
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更新日期：2015-09-15 00:00:00
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更新日期：2020-09-07 00:00:00
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
doi：10.1186/s12974-019-1586-1
更新日期：2019-10-17 00:00:00
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
doi：10.1186/1742-2094-5-4
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
doi：10.1186/s12974-016-0487-9
更新日期：2016-01-27 00:00:00
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
doi：10.1186/s12974-015-0441-2
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章
doi：10.1186/s12974-015-0381-x
更新日期：2015-10-06 00:00:00
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journal_title：Journal of neuroinflammation
pub_type： 杂志文章,评审
doi：10.1186/1742-2094-7-9
更新日期：2010-01-29 00:00:00
abstract：BACKGROUND:Synucleinopathies comprise a group of neurodegenerative diseases associated with abnormal accumulation of α-synuclein. One of the key factors that contribute to the progression of synucleinopathies is neuroinflammation. However, the role of lymphocytes in synucleinopathies like Parkinson's disease (PD) remai...
journal_title：Journal of neuroinflammation
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doi：10.1186/s12974-016-0632-5
更新日期：2016-06-30 00:00:00
