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Titolo:
IL-6-DEFICIENT MICE RESIST MYELIN OLIGODENDROCYTE GLYCOPROTEIN-INDUCED AUTOIMMUNE ENCEPHALOMYELITIS
Autore:
EUGSTER HP; FREI K; KOPF M; LASSMANN H; FONTANA A;
Indirizzi:
UNIV ZURICH HOSP,DEPT INTERNAL MED,CLIN IMMUNOL SECT,HAELDELIWEG 4 CH-8044 ZURICH SWITZERLAND UNIV ZURICH HOSP,DEPT NEUROSURG CH-8091 ZURICH SWITZERLAND BASEL INST IMMUNOL BASEL SWITZERLAND UNIV VIENNA,INST NEUROL A-1010 VIENNA AUSTRIA
Titolo Testata:
European Journal of Immunology
fascicolo: 7, volume: 28, anno: 1998,
pagine: 2178 - 2187
SICI:
0014-2980(1998)28:7<2178:IMRMOG>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; TUMOR-NECROSIS-FACTOR; INTERLEUKIN-6-DEFICIENT MICE; MONOCLONAL-ANTIBODY; TRANSGENIC MICE; T-CELLS; ADHESION; EXPRESSION; DISEASE;
Keywords:
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; IL-6; MYELIN OLIGODENDROCYTE GLYCOPROTEIN; AUTOIMMUNITY; VCAM-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
H.P. Eugster et al., "IL-6-DEFICIENT MICE RESIST MYELIN OLIGODENDROCYTE GLYCOPROTEIN-INDUCED AUTOIMMUNE ENCEPHALOMYELITIS", European Journal of Immunology, 28(7), 1998, pp. 2178-2187

Abstract

Experimental autoimmune encephalomyelitis (EAE) is induced by immunization with myelin components including myelin oligodendrocyte glycoprotein (MOG). Myelin-specific Th1 cells enter the central nervous system(CNS) via binding of very late antigen 4 (VLA-4) to the endothelial vascular cell adhesion molecule 1 (VCAM-1). In the present study, mice with a homologous disruption of the gene encoding IL-6 are found to beresistant to MOG-induced EAE as evidenced by absence of clinical symptoms, minimal infiltration of CD3+ T cells and monocytes into the CNS and lack of demyelination. The failure to induce EAE in IL-6(-/-) miceis not due to the absence of priming, since lymphocytes of immunized IL-6(-/-) mice proliferate in response to MOG and produce pro-inflammatory cytokines including IL-2 and IFN-gamma. However, in MOG-immunizedIL-6(-/-) mice, serum anti-MOG antibody titers were found to be drastically reduced. This observation is unlikely to be responsible for resistance to EAE, because B cell-deficient (mu MT) mice proved to be fully susceptible to the disease. A striking difference between MOG-immunized wild-type (wt) and IL-6(-/-) mice was the expression of endothelial VCAM-1 and ICAM-1, which were dramatically up-regulated in the CNS in wt but not in IL-6(-/-) mice. Taking into account recent studies onthe role of VCAM-1 in the entry of Th1 cells into the CNS, the absence of VCAM-1 on endothelial cells in IL-6(-/-) mice may explain their resistance to EAE.

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Documento generato il 27/01/21 alle ore 02:47:26