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Titolo:
T-cell-based immunity counteracts the potential toxicity of glutamate in the central nervous system
Autore:
Schori, H; Yoles, E; Schwartz, M;
Indirizzi:
Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel Weizmann Inst Sci Rehovot Israel IL-76100 biol, IL-76100 Rehovot, Israel
Titolo Testata:
JOURNAL OF NEUROIMMUNOLOGY
fascicolo: 2, volume: 119, anno: 2001,
pagine: 199 - 204
SICI:
0165-5728(20011001)119:2<199:TICTPT>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
NEUROLOGICAL DISORDERS; OXIDATIVE STRESS; OPTIC-NERVE; EXCITOTOXICITY; BRAIN; NEUROTRANSMITTER; TRANSPORTERS; GLAUCOMA; NEURONS; DEATH;
Keywords:
beneficial autoimmunity; neuroprotection; CNS injury; glutamate toxicity; oxidative stress; CNS degeneration;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Schwartz, M Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel Weizmann Inst Sci Rehovot Israel IL-76100 00 Rehovot, Israel
Citazione:
H. Schori et al., "T-cell-based immunity counteracts the potential toxicity of glutamate in the central nervous system", J NEUROIMM, 119(2), 2001, pp. 199-204

Abstract

Injuries to the central nervous system (CNS) evoke self-destructive processes, which eventually lead to a much greater loss of tissue than that caused by the trauma itself. The agents of self-destruction include physiological compounds, such as glutamate, which are essential for the proper functioning of the CNS, but become cytotoxic when their normal concentrations are exceeded. The CNS is equipped with buffering mechanisms that are specific for each compound. Here we show, using Balb/c mice (a strain resistant to induction of experimental autoimmune encephalomyclitis), that after intravitreal injection of any concentration of glutamate (a neurotransmitter that becomes toxic when in excess) or ammonium-ferrous sulfate hexahydrate (which increases the formation of toxic oxygen species), the loss of retinal ganglion cells in mice devoid of mature T cells (nude mice) is significantly greater than in matched wild-type controls. We further show that this outcome can be partially reversed by supplying the T cell-defective mice with splenocytes, derived from the wild-type mice. The results suggest that potentially toxic physiological compounds, when present in excessive amounts, can recruit and activate a T-cell-dependent self-protective immune mechanism. Thismay represent a prototype mechanism for the physiological regulation of potentially destructive CNS events by T-cell-mediated immune activity, when the local buffering mechanisms cannot adequately cope with them. (C) 2001 Elsevier Science B.V.. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/01/20 alle ore 18:36:46