Journal of neuroimmunology
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The stiff person syndrome (SPS) is a CNS disorder of putative autoimmune aetiology, which is clinically characterized by severe rigidity and spasms. In most cases, SPS is associated with serum antibodies against glutamic acid decarboxylase (GAD-Ab). Recent studies suggested that GAD-Ab might be directly involved in the pathogenesis of SPS. Further support for this hypothesis would come from studies providing qualitative evidence for the presence of GAD-Ab-producing B cell clones within the CNS of patients with SPS. ⋯ Here we demonstrate for the first time that IgG OCBs in SPS bind GAD. Our findings contribute to the ongoing discussion on whether the autoimmune process against GAD is involved in the pathogenesis of SPS by indicating that anti-GAD-Ab is produced by B cell clones within the CNS.
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In a large proportion of individuals nervous system damage may lead to a debilitating chronic neuropathic pain. Such pain may now be considered a neuro-immune disorder, since recent data indicate a critical involvement of innate and adaptive immune responses following nerve injury. Activation of immune and immune-like glial cells in the injured nerve, dorsal root ganglia and spinal cord results in the release of both pro- and anti-inflammatory cytokines, as well as algesic and analgesic mediators, the balance of which determines whether pain chronicity is established. This review will critically examine the role of the immune system in modulating chronic pain in animal models of nervous system injury, and highlight the possible therapeutic opportunities to intervene in the development and maintenance of neuropathic pain.
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Comparative Study
Therapeutic effects of resveratrol during acute periods following experimental ischemic stroke.
We defined whether resveratrol administration during the acute phase of ischemic stroke reduces brain injury in mice. Infarct volumes were decreased significantly in both sexes with different doses of resveratrol (5mg/kg for males and 1mg/kg for females) administered 3h after ischemic stroke. ⋯ Resveratrol suppressed expressions of IL-1β and TNF-α, microglial activation, and ROS production in the ischemic cortex. The findings suggest that the suppression of inflammation is partly associated with the neuroprotective effects of resveratrol, and resveratrol can be developed as a therapeutic drug for acute ischemic stroke.
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Antiganglioside antibodies play a pathogenic role in the pathophysiology of Guillain-Barré syndrome (GBS) and Fisher syndrome (FS). Antiganglioside antibody-mediated nerve injury is likely to result from nerve damage through complement activation or dysfunction of molecules such as voltage-gated sodium and calcium channels. ⋯ The glycolipid environment or the specific distribution of target gangliosides in the peripheral nervous system may also influence the pathogenic effect of antiganglioside antibodies in GBS and FS. Structural and functional analyses of glycoepitopes of ganglioside complexes in membranes will provide new vistas on antibody-antigen interaction in GBS and shed light on microdomain function mediated by carbohydrate-carbohydrate interactions, which may lead to novel treatments for GBS and FS.
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Multicenter Study Comparative Study
Anti-myelin antibodies modulate clinical expression of childhood multiple sclerosis.
Anti-myelin basic protein (MBP) antibodies in pediatric-onset MS and controls were characterized. Serum samples were obtained from 94 children with MS and 106 controls. Paired CSF and serum were obtained from 25 children with MS at time of their initial episode of acute demyelinating syndrome (ADS). ⋯ Serum levels of anti-MBP antibodies correlated significantly with their CSF levels, and their presence in children with MS was associated with significantly increased risk of an acute disseminated encephalomyelitis-like initial clinical presentation. While antibodies to both immature and mature forms of MBP can be present as part of the normal pediatric humoral repertoire, these anti-myelin antibodies are of surprisingly high affinity, can access the CNS during inflammation, and have the capacity to modulate disease expression. Our findings identify an immune mechanism that could contribute to the observed heterogeneity in spectrum of clinical presentations in early-onset MS.