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Towards neuroimmunotherapy for cancer: the neurotransmitters glutamate, dopamine and GnRH-II augment substantially the ability of T cells of few head and neck cancer patients to perform spontaneous migration, chemotactic migration and migration towards the autologous tumor, and also elevate markedly the expression of CD3zeta and CD3epsilon TCR-associated chains.
Saussez S, Laumbacher B, Chantrain G, Rodriguez A, Gu S, Wank R, Levite M. Saussez S, et al. Among authors: levite m. J Neural Transm (Vienna). 2014 Aug;121(8):1007-27. doi: 10.1007/s00702-014-1242-y. Epub 2014 Jul 17. J Neural Transm (Vienna). 2014. PMID: 25030361
Normal human CD4(+) helper T cells express Kv1.1 voltage-gated K(+) channels, and selective Kv1.1 block in T cells induces by itself robust TNFα production and secretion and activation of the NFκB non-canonical pathway.
Fellerhoff-Losch B, Korol SV, Ganor Y, Gu S, Cooper I, Eilam R, Besser M, Goldfinger M, Chowers Y, Wank R, Birnir B, Levite M. Fellerhoff-Losch B, et al. Among authors: levite m. J Neural Transm (Vienna). 2016 Mar;123(3):137-57. doi: 10.1007/s00702-015-1446-9. Epub 2015 Nov 26. J Neural Transm (Vienna). 2016. PMID: 26611796
Glutamate, T cells and multiple sclerosis.
Levite M. Levite M. J Neural Transm (Vienna). 2017 Jul;124(7):775-798. doi: 10.1007/s00702-016-1661-z. Epub 2017 Feb 24. J Neural Transm (Vienna). 2017. PMID: 28236206 Review.
Dopamine, T cells and multiple sclerosis (MS).
Levite M, Marino F, Cosentino M. Levite M, et al. J Neural Transm (Vienna). 2017 May;124(5):525-542. doi: 10.1007/s00702-016-1640-4. Epub 2017 Mar 10. J Neural Transm (Vienna). 2017. PMID: 28283756 Review.
Glutamate receptor antibodies in neurological diseases: anti-AMPA-GluR3 antibodies, anti-NMDA-NR1 antibodies, anti-NMDA-NR2A/B antibodies, anti-mGluR1 antibodies or anti-mGluR5 antibodies are present in subpopulations of patients with either: epilepsy, encephalitis, cerebellar ataxia, systemic lupus erythematosus (SLE) and neuropsychiatric SLE, Sjogren's syndrome, schizophrenia, mania or stroke. These autoimmune anti-glutamate receptor antibodies can bind neurons in few brain regions, activate glutamate receptors, decrease glutamate receptor's expression, impair glutamate-induced signaling and function, activate blood brain barrier endothelial cells, kill neurons, damage the brain, induce behavioral/psychiatric/cognitive abnormalities and ataxia in animal models, and can be removed or silenced in some patients by immunotherapy.
Levite M. Levite M. J Neural Transm (Vienna). 2014 Aug;121(8):1029-75. doi: 10.1007/s00702-014-1193-3. Epub 2014 Aug 1. J Neural Transm (Vienna). 2014. PMID: 25081016 Review.
58 results