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Negative regulation of autoimmune demyelination by the inhibitory receptor CLM-1

Multiple sclerosis and its preclinical model, experimental autoimmune encephalomyelitis, are marked by perivascular inflammation and demyelination. Myeloid cells, derived from circulating progenitors, are a prominent component of the inflammatory infiltrate and are believed to directly contribute to...

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Autores principales: Xi, Hongkang, Katschke, Kenneth J., Helmy, Karim Y., Wark, Paige A., Kljavin, Noelyn, Clark, Hilary, Eastham-Anderson, Jeffrey, Shek, Theresa, Roose-Girma, Merone, Ghilardi, Nico, van Lookeren Campagne, Menno
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812551/
https://www.ncbi.nlm.nih.gov/pubmed/20038601
http://dx.doi.org/10.1084/jem.20091508
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author Xi, Hongkang
Katschke, Kenneth J.
Helmy, Karim Y.
Wark, Paige A.
Kljavin, Noelyn
Clark, Hilary
Eastham-Anderson, Jeffrey
Shek, Theresa
Roose-Girma, Merone
Ghilardi, Nico
van Lookeren Campagne, Menno
author_facet Xi, Hongkang
Katschke, Kenneth J.
Helmy, Karim Y.
Wark, Paige A.
Kljavin, Noelyn
Clark, Hilary
Eastham-Anderson, Jeffrey
Shek, Theresa
Roose-Girma, Merone
Ghilardi, Nico
van Lookeren Campagne, Menno
author_sort Xi, Hongkang
collection PubMed
description Multiple sclerosis and its preclinical model, experimental autoimmune encephalomyelitis, are marked by perivascular inflammation and demyelination. Myeloid cells, derived from circulating progenitors, are a prominent component of the inflammatory infiltrate and are believed to directly contribute to demyelination and axonal damage. How the cytotoxic activity of these myeloid cells is regulated is poorly understood. We identify CMRF-35–like molecule-1 (CLM-1) as a negative regulator of autoimmune demyelination. CLM-1 is expressed on inflammatory myeloid cells present in demyelinating areas of the spinal cord after immunization of mice with MOG(35-55) (myelin oligodendrocyte glycoprotein) peptide. Absence of CLM-1 resulted in significantly increased nitric oxide and proinflammatory cytokine production, along with increased demyelination and worsened clinical scores, whereas T cell responses in the periphery or in the spinal cord remained unaffected. This study thus identifies CLM-1 as a negative regulator of myeloid effector cells in autoimmune demyelination.
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spelling pubmed-28125512010-07-18 Negative regulation of autoimmune demyelination by the inhibitory receptor CLM-1 Xi, Hongkang Katschke, Kenneth J. Helmy, Karim Y. Wark, Paige A. Kljavin, Noelyn Clark, Hilary Eastham-Anderson, Jeffrey Shek, Theresa Roose-Girma, Merone Ghilardi, Nico van Lookeren Campagne, Menno J Exp Med Brief Definitive Report Multiple sclerosis and its preclinical model, experimental autoimmune encephalomyelitis, are marked by perivascular inflammation and demyelination. Myeloid cells, derived from circulating progenitors, are a prominent component of the inflammatory infiltrate and are believed to directly contribute to demyelination and axonal damage. How the cytotoxic activity of these myeloid cells is regulated is poorly understood. We identify CMRF-35–like molecule-1 (CLM-1) as a negative regulator of autoimmune demyelination. CLM-1 is expressed on inflammatory myeloid cells present in demyelinating areas of the spinal cord after immunization of mice with MOG(35-55) (myelin oligodendrocyte glycoprotein) peptide. Absence of CLM-1 resulted in significantly increased nitric oxide and proinflammatory cytokine production, along with increased demyelination and worsened clinical scores, whereas T cell responses in the periphery or in the spinal cord remained unaffected. This study thus identifies CLM-1 as a negative regulator of myeloid effector cells in autoimmune demyelination. The Rockefeller University Press 2010-01-18 /pmc/articles/PMC2812551/ /pubmed/20038601 http://dx.doi.org/10.1084/jem.20091508 Text en © 2010 Xi et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Brief Definitive Report
Xi, Hongkang
Katschke, Kenneth J.
Helmy, Karim Y.
Wark, Paige A.
Kljavin, Noelyn
Clark, Hilary
Eastham-Anderson, Jeffrey
Shek, Theresa
Roose-Girma, Merone
Ghilardi, Nico
van Lookeren Campagne, Menno
Negative regulation of autoimmune demyelination by the inhibitory receptor CLM-1
title Negative regulation of autoimmune demyelination by the inhibitory receptor CLM-1
title_full Negative regulation of autoimmune demyelination by the inhibitory receptor CLM-1
title_fullStr Negative regulation of autoimmune demyelination by the inhibitory receptor CLM-1
title_full_unstemmed Negative regulation of autoimmune demyelination by the inhibitory receptor CLM-1
title_short Negative regulation of autoimmune demyelination by the inhibitory receptor CLM-1
title_sort negative regulation of autoimmune demyelination by the inhibitory receptor clm-1
topic Brief Definitive Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812551/
https://www.ncbi.nlm.nih.gov/pubmed/20038601
http://dx.doi.org/10.1084/jem.20091508
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