Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules

Gerd Meyer zu Hörste, Anne K. Mausberg, Johanna I. Müller, Helmar C. Lehmann, Stefan Löber, Peter Gmeiner, Hans Peter Hartung, Olaf Stüve, Carsten Korth, Bernd C. Kieseier

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


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.

Original languageEnglish (US)
Article numbere21223
JournalPloS one
Issue number6
StatePublished - 2011

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • General


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