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GABAergic signalling in the immune system
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. Karolinska Institutet, Sweden.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. Karolinska Institutet, Sweden.
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2015 (English)In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 213, no 4, 819-827 p.Article, review/survey (Refereed) Published
Abstract [en]

The GABAergic system is the main inhibitory neurotransmitter system in the central nervous system (CNS) of vertebrates. Signalling of the transmitter c-aminobutyric acid (GABA) via GABA type A receptor channels or G-protein-coupled type B receptors is implicated in multiple CNS functions. Recent findings have implicated the GABAergic system in immune cell functions, inflammatory conditions and diseases in peripheral tissues. Interestingly, the specific effects may vary between immune cell types, with stage of activation and be altered by infectious agents. GABA/GABA-A receptor-mediated immunomodulatory functions have been unveiled in immune cells, being present in T lymphocytes and regulating the migration of Toxoplasma-infected dendritic cells. The GABAergic system may also play a role in the regulation of brain resident immune cells, the microglial cells. Activation of microglia appears to regulate the function of GABAergic neurotransmission in neighbouring neurones through changes induced by secretion of brain-derived neurotrophic factor. The neurotransmitter-driven immunomodulation is a new but rapidly growing field of science. Herein, we review the present knowledge of the GABA signalling in immune cells of the periphery and the CNS and raise questions for future research.

Place, publisher, year, edition, pages
2015. Vol. 213, no 4, 819-827 p.
Keyword [en]
dendritic cell, GABA, GABA-A, glutamic acid decarboxylase, microglia, T cell
National Category
Physiology
Identifiers
URN: urn:nbn:se:su:diva-116776DOI: 10.1111/apha.12467ISI: 000351208100011PubMedID: 25677654OAI: oai:DiVA.org:su-116776DiVA: diva2:808221
Note

AuthorCount:5;

Available from: 2015-04-27 Created: 2015-04-27 Last updated: 2017-12-04Bibliographically approved

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