ArticlePloS one2011
Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Unveiling the Role of Schwann Cell Plasticity in the Pathogenesis of Diabetic Peripheral Neuropathy.International journal of molecular sciences · 2024Review
- Immune Modifying Effect of Drug Free Biodegradable Nanoparticles on Disease Course of Experimental Autoimmune Neuritis.Pharmaceutics · 2022Article
- Current and Emerging Pharmacotherapeutic Interventions for the Treatment of Peripheral Nerve Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Concurrent leukoencephalomyelitis and polyneuritis in a Maltese terrier: resembling combined central and peripheral demyelination in humans.The Journal of veterinary medical science · 2019Article
- Novel pathomechanisms in inflammatory neuropathies.Journal of neuroinflammation · 2017Review
- Schwann cells promote post-traumatic nerve inflammation and neuropathic pain through MHC class II.Scientific reports · 2017Article
- Dissecting the Role of Anti-ganglioside Antibodies in Guillain-Barré Syndrome: an Animal Model Approach.Molecular neurobiology · 2016Review
Corrections and comments
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Authors and funding
10 authors.
Funding
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Abstract
Activation of inflammatory cells is central to the pathogenesis of autoimmune demyelinating diseases of the peripheral nervous system. The novel chimeric compound quinpramine--generated from imipramine and quinacrine--redistributes cholesterol rich membrane domains to intracellular compartments. We studied the immunological and clinical effects of quinpramine in myelin homogenate induced Lewis rat experimental autoimmune neuritis (EAN), a model system for acute human inflammatory neuropathies, such as the Guillain-Barré syndrome. EAN animals develop paresis of all limbs due to autoimmune inflammation of peripheral nerves. Quinpramine treatment ameliorated clinical disease severity of EAN and infiltration of macrophages into peripheral nerves. It reduced expression of MHC class II molecules on antigen presenting cells and antigen specific T cell proliferation both in vitro and in vivo. Quinpramine exerted its anti-proliferatory effect on antigen presenting cells, but not on responder T cells. Our data suggest that quinpramine represents a candidate pharmaceutical for inflammatory neuropathies.
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