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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/8454

Title: Molecular evidence of glycine receptors on macrophages: A possible relationship with multiple sclerosis
Authors: Carmans, Sofie
Hendriks, Jerome J. A.
Rigo, Jean-Michel
Stinissen, Piet
Hellings, Niels
Issue Date: 2008
Citation: JOURNAL OF NEUROIMMUNOLOGY, 197(2). p. 174-174
Abstract: Glycine plays an important role in mediating fast inhibitory neurotransmission within the central nervous system (CNS). Outside the CNS, the glycine receptor (GlyR) is present on various immune cells such as neutrophils, lymphocytes and alveolar macrophages. In that respect, glycine is protective in several animal models of peripheral inflammation. Such an immunomodulatory role might be of importance for neuroinflammatory diseases such as multiple sclerosis (MS). Although glycine levels are increased in plasma and cerebrospinal fluid of MS patients, the exact role of glycine on the disease process has not been studied so far. In this study, the effect of glycine on macrophages, the most important effector cells in MS, is investigated. Therefore, mouse and rat macrophage cell lines, primary isolated peritoneal macrophages and rat microglial cells are used. Initial experiments show that macrophages and microglia express various a subunits of the GlyR (a1 and a2), the beta subunit and gephyrin, a GlyR associated protein, on both mRNA and protein level. Furthermore, macrophages as well as microglia express the glycine transporter GLYT1. Currently we investigate whether glycine affects macrophage function. Initial experiments show that glycine modulates the production of pro-inflammatory mediators by macrophages and may thereby influence neuroinflammatory responses during MS.
Publication appears at doi: 10.1016/j.jneuroim.2008.04.005
Notes: Hasselt Univ, Biomed Res Inst, Diepenbeek, Belgium. Transnatl Univ Limburg, Sch Life Sci, Diepenbeek, Belgium.
URI: http://hdl.handle.net/1942/8454
ISI #: 000258388700113
ISSN: 0165-5728
Category: M
Type: Journal Contribution
Appears in Collections: Research publications

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