Keio University · Medicine
Professor Shigeaki Suzuki's research lab specializes in neuroimmunology and inflammatory myopathies, focusing on the pathogenesis, serological markers, and cytokine involvement in autoimmune neurological disorders. The lab investigates autoantibodies such as anti-SRP and anti-HMGCR in immune-mediated necrotizing myopathy and antisynthetase syndrome, exploring their clinical and histological correlations. A key focus is on the role of pro-inflammatory and neurotrophic cytokines—particularly interleukin-6 (IL-6)—in central nervous system disorders, including stroke, where IL-6's dual role in neuroinflammation and repair is being dissected at the cellular and spatial level. The lab employs advanced immunohistochemical and molecular techniques to map cytokine expression and cellular sources in experimental models of cerebral ischemia.
Figures are computed from collected data and may differ slightly.
The prompt and correct recognition of MG following treatment with immune checkpoint inhibitors in patients with cancer is important.
Anti-SRP antibodies are associated with severe neurological symptoms, more so than are anti-HMGCR antibodies. Although these autoantibodies are independent serological markers associated with IMNM, patients bearing either share common characteristics.
Interleukin-6 (IL-6) is pleiotropic cytokine involved in many central nervous system disorders including stroke, and elevated serum IL-6 has been found in acute stroke patients. IL-6 is implicated in the inflammation, which contributes to both injury and repair process after cerebral ischemia. However, IL-6 is one of the neurotrophic cytokines sharing a common receptor subunit, gp130, with other neurotrophic cytokines, such as leukemia inhibitory factor (LIF) and ciliary neurotrophic factor. The
Anti-SRP antibodies are associated with different clinical courses and histological presentations.
Although clinical presentations of antisynthetase syndrome were relatively homogeneous, anti-OJ antibodies were associated with severe muscle involvement. Antisynthetase syndrome is a clinical and histological subset among idiopathic inflammatory myopathies.
Although interleukin-6 (IL-6) has various neuroprotective effects against cerebral ischemia, the topographic distribution and cellular source of IL-6 after cerebral ischemia remain unclear. In the current study, the localization of IL-6 protein was immunohistochemically examined in rats after 3.5, 12, 24, and 48 hours of reperfusion after 1.5 hours of middle cerebral artery occlusion. Middle cerebral artery occlusion was induced by the intraluminal suture method. The specificity of the anti-IL-6
A subset of patients with anti-SRP myopathy can show a chronic progressive form associated with severe clinical deficits.
Myasthenia gravis (MG) is caused by antibodies that react mainly with the acetylcholine receptor on the postsynaptic site of the neuromuscular junction. A wide range of clinical presentations and associated features allow MG to be classified into subtypes based on autoantibody status. Striational antibodies, which react with epitopes on the muscle proteins titin, ryanodine receptor (RyR), and Kv1.4, are frequently found in MG patients with late-onset and thymoma. Antititin and anti-RyR antibodie
It has been demonstrated that anti-Kv1.4 antibodies are possible markers for cardiac involvements in MG patients.
Statins have a variety of myotoxic effects and can trigger the development of inflammatory myopathies or myasthenia gravis (MG) mediated by immunomodulatory properties. Autoantibodies to 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) have been identified in patients with statin-associated myopathy. The purpose of the present study is to develop an enzyme-linked immunosorbent assay (ELISA) of anti-HMGCR antibodies and to elucidate the clinical significance of anti-HMGCR antibodies in Jap
Anti-SRP antibody is useful for discriminating PM from MD among patients with myopathies.
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