Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules.
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...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2011-01-01
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| Series: | PLoS ONE |
| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21698177/?tool=EBI |
| _version_ | 1818845105201610752 |
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| author | 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 |
| author_facet | 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 |
| author_sort | Gerd Meyer zu Hörste |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-19T05:24:22Z |
| format | Article |
| id | doaj.art-c25d308f220f4236916dec59160e4b9f |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-19T05:24:22Z |
| publishDate | 2011-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-c25d308f220f4236916dec59160e4b9f2022-12-21T20:34:24ZengPublic Library of Science (PLoS)PLoS ONE1932-62032011-01-0166e2122310.1371/journal.pone.0021223Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules.Gerd Meyer zu HörsteAnne K MausbergJohanna I MüllerHelmar C LehmannStefan LöberPeter GmeinerHans-Peter HartungOlaf StüveCarsten KorthBernd C KieseierActivation 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.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21698177/?tool=EBI |
| spellingShingle | 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 Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules. PLoS ONE |
| title | Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules. |
| title_full | Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules. |
| title_fullStr | Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules. |
| title_full_unstemmed | Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules. |
| title_short | Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules. |
| title_sort | quinpramine ameliorates rat experimental autoimmune neuritis and redistributes mhc class ii molecules |
| url | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21698177/?tool=EBI |
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