TRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation.

TRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation.

TRPM2, a highly Ca(2+)-permeable member of the transient receptor potential melastatin-related (TRPM) family of cation channels, is expressed in cells of the immune system. We demonstrate firstly that TRPM2 cation channels on T cells critically influence T cell proliferation and proinflammatory cyto...

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Autores principales: Nico Melzer, Gordon Hicking, Kerstin Göbel, Heinz Wiendl
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2012
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Acceso en línea:https://doaj.org/article/8ec43f6a7756479ab0d4eddd781a2f08
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spelling oai:doaj.org-article:8ec43f6a7756479ab0d4eddd781a2f082021-11-18T08:12:09ZTRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation.1932-620310.1371/journal.pone.0047617https://doaj.org/article/8ec43f6a7756479ab0d4eddd781a2f082012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23077651/?tool=EBIhttps://doaj.org/toc/1932-6203TRPM2, a highly Ca(2+)-permeable member of the transient receptor potential melastatin-related (TRPM) family of cation channels, is expressed in cells of the immune system. We demonstrate firstly that TRPM2 cation channels on T cells critically influence T cell proliferation and proinflammatory cytokine secretion following polyclonal T cell receptor stimulation. Consistently, trpm2-deficient mice exhibited an attenuated clincal phenotype of experimental autoimmune encephalomyelitis (EAE) with reduced inflammatory and demyelinating spinal cord lesions. Importantly, trmp2-deficient T cells were as susceptible as wildtype T cells to oxidative stress-induced cell death as it occurs in inflammatory CNS lesions. This supports the notion that the attenuated EAE phenotype is mainly due to reduced T cell effector functions but unaffected by potential modulation of T cell survival at the site of inflammation. Our findings suggest TRPM2 cation channels as a potential target for treating autoimmune CNS inflammation.Nico MelzerGordon HickingKerstin GöbelHeinz WiendlPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 10, p e47617 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Nico Melzer
Gordon Hicking
Kerstin Göbel
Heinz Wiendl
TRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation.
description TRPM2, a highly Ca(2+)-permeable member of the transient receptor potential melastatin-related (TRPM) family of cation channels, is expressed in cells of the immune system. We demonstrate firstly that TRPM2 cation channels on T cells critically influence T cell proliferation and proinflammatory cytokine secretion following polyclonal T cell receptor stimulation. Consistently, trpm2-deficient mice exhibited an attenuated clincal phenotype of experimental autoimmune encephalomyelitis (EAE) with reduced inflammatory and demyelinating spinal cord lesions. Importantly, trmp2-deficient T cells were as susceptible as wildtype T cells to oxidative stress-induced cell death as it occurs in inflammatory CNS lesions. This supports the notion that the attenuated EAE phenotype is mainly due to reduced T cell effector functions but unaffected by potential modulation of T cell survival at the site of inflammation. Our findings suggest TRPM2 cation channels as a potential target for treating autoimmune CNS inflammation.
format article
author Nico Melzer
Gordon Hicking
Kerstin Göbel
Heinz Wiendl
author_facet Nico Melzer
Gordon Hicking
Kerstin Göbel
Heinz Wiendl
author_sort Nico Melzer
title TRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation.
title_short TRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation.
title_full TRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation.
title_fullStr TRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation.
title_full_unstemmed TRPM2 cation channels modulate T cell effector functions and contribute to autoimmune CNS inflammation.
title_sort trpm2 cation channels modulate t cell effector functions and contribute to autoimmune cns inflammation.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/8ec43f6a7756479ab0d4eddd781a2f08
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AT gordonhicking trpm2cationchannelsmodulatetcelleffectorfunctionsandcontributetoautoimmunecnsinflammation
AT kerstingobel trpm2cationchannelsmodulatetcelleffectorfunctionsandcontributetoautoimmunecnsinflammation
AT heinzwiendl trpm2cationchannelsmodulatetcelleffectorfunctionsandcontributetoautoimmunecnsinflammation
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