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Titolo:
Neuronal survival after CNS insult is determined by a genetically encoded autoimmune response
Autore:
Kipnis, J; Yoles, E; Schori, H; Hauben, E; Shaked, I; 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 NEUROSCIENCE
fascicolo: 13, volume: 21, anno: 2001,
pagine: 4564 - 4571
SICI:
0270-6474(20010701)21:13<4564:NSACII>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; TRAUMATIC BRAIN INJURY; SPINAL-CORD CONTUSION; REGULATORY T-CELLS; MOUSE STRAINS; OPTIC-NERVE; TORPEDO-CALIFORNICA; MYASTHENIA-GRAVIS; IMMUNE PRIVILEGE;
Keywords:
protective autoimmunity; encephalitogenicity; neuroprotection; autoimmune disease; CNS; EAE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
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:
J. Kipnis et al., "Neuronal survival after CNS insult is determined by a genetically encoded autoimmune response", J NEUROSC, 21(13), 2001, pp. 4564-4571

Abstract

Injury to the CNS is often followed by a spread of damage (secondary degeneration), resulting in neuronal losses that are substantially greater than might have been predicted from the severity of the primary insult. Studies in our laboratory have shown that injured CNS neurons can benefit from active or passive immunization with CNS myelin-associated antigens. The fact that autoimmune T-cells can be both beneficial and destructive, taken together with the established phenomenon of genetic predisposition to autoimmune diseases, raises the question: will genetic predisposition to autoimmune diseases affect the outcome of traumatic insult to the CNS? Here we show that the survival rate of retinal ganglion cells in adult mice or rats after crush injury of the optic nerve or intravitreal injection of a toxic dosage ofglutamate is up to twofold higher in strains that are resistant to the CNSautoimmune disease experimental autoimmune encephalomyelitis (EAE) than insusceptible strains. The difference was found to be attributed, at least in part, to a beneficial T-cell response that was spontaneously evoked afterCNS insult in the resistant but not in the susceptible strains. In animalsof EAE-resistant but not of EAE-susceptible strains devoid of mature T-cells (as a result of having undergone thymectomy at birth), the numbers of surviving neurons after optic nerve injury were significantly lower (by 60%) than in the corresponding normal animals. Moreover, the rate of retinal ganglion cell survival was higher when the optic nerve injury was preceded by an unrelated CNS (spinal cord) injury in the resistant strains but not in the susceptible strains. It thus seems that, in normal animals of EAE-resistant strains (but not of susceptible strains), the injury evokes an endogenous protective response that is T-cell dependent. These findings imply that a protective T-cell-dependent response and resistance to autoimmune diseaseare regulated by a common mechanism. The results of this study compel us to modify our understanding of autoimmunity and autoimmune diseases, as wellas the role of autoimmunity in non-autoimmune CNS disorders. They also obviously have far-reaching clinical implications in terms of prognosis and individual therapy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 10:00:29