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...

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Autores principales:	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
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c25d308f220f4236916dec59160e4b9f
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spelling	oai:doaj.org-article:c25d308f220f4236916dec59160e4b9f2021-11-18T06:51:56ZQuinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules.1932-620310.1371/journal.pone.0021223https://doaj.org/article/c25d308f220f4236916dec59160e4b9f2011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21698177/?tool=EBIhttps://doaj.org/toc/1932-6203Activation 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.Gerd Meyer zu HörsteAnne K MausbergJohanna I MüllerHelmar C LehmannStefan LöberPeter GmeinerHans-Peter HartungOlaf StüveCarsten KorthBernd C KieseierPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 6, p e21223 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q 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.
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.
format	article
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
title	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_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_sort	quinpramine ameliorates rat experimental autoimmune neuritis and redistributes mhc class ii molecules.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/c25d308f220f4236916dec59160e4b9f
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Quinpramine ameliorates rat experimental autoimmune neuritis and redistributes MHC class II molecules.

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