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Titolo:
Severity of symptoms and demyelination in MOG-induced EAE depends on TNFR1
Autore:
Eugster, HP; Frei, K; Bachmann, R; Bluethmann, H; Lassmann, H; Fontana, A;
Indirizzi:
UnivtzerlandHosp, Dept Internal Med, Clin Immunol Sect, CH-8044 Zurich, Swi Univ Zurich Hosp Zurich Switzerland CH-8044 ol Sect, CH-8044 Zurich, Swi Univ Zurich Hosp, Dept Neurosurg, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 CH-8091 Zurich, Switzerland Univ Vienna, Neurol Inst, A-1010 Vienna, Austria Univ Vienna Vienna Austria A-1010 a, Neurol Inst, A-1010 Vienna, Austria F Hoffmann LaRoche Ltd, CNS Dept, Basel, Switzerland F Hoffmann LaRoche Ltd Basel Switzerland , CNS Dept, Basel, Switzerland
Titolo Testata:
EUROPEAN JOURNAL OF IMMUNOLOGY
fascicolo: 2, volume: 29, anno: 1999,
pagine: 626 - 632
SICI:
0014-2980(199902)29:2<626:SOSADI>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; PERIPHERAL LYMPHOID ORGANS; MULTIPLE-SCLEROSIS; PATCH ORGANOGENESIS; LYMPHOTOXIN-ALPHA; FACTOR RECEPTOR-1; MICE DEFICIENT;
Keywords:
autoimmunity; tumor necrosis factor; inflammation; knockout; neuroimmunology;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Eugster, HP Univ044rich Hosp, Dept Internal Med, Clin Immunol Sect, Haeldeliweg 4, CH-8 Univ Zurich Hosp Haeldeliweg 4 Zurich Switzerland CH-8044 H-8
Citazione:
H.P. Eugster et al., "Severity of symptoms and demyelination in MOG-induced EAE depends on TNFR1", EUR J IMMUN, 29(2), 1999, pp. 626-632

Abstract

The individual role of tumor necrosis factor receptor 1 (TNFR1) and TNFR2 signaling in experimental autoimmune encephalomeylitis (EAE) was investigated using mice lacking TNFR1 (TNFR1-/-), TNFR2 (TNFR2-/-) as well as double receptor (TNFR1/2-/-) and double ligand (TNF/LT alpha-/-) knockout mice. inwild-type (wt) mice immunized with myelin oligodendrocyte glycoprotein (MOG) peptide 35-55 the clinical course is characterized by an acute disease onset with peak disease scores and a consecutive chronic phase lasting up to60 days. Compared to control mice, TNF/LT alpha-deficient mice showed a significant delay in disease onset and a remarkable reduction in demyelination which was, however, associated with increased inflammation. In TNFR1-/- and TNFR1/2-/- mice, the disease course was comparable to TNF/LT alpha-deficient mice but rather monophasic and less severe at late time points. Likewise only minimal spinal cord demyelination became apparent. In contrast, thecourse of EAE in TNFR2-/- mice was severe and associated with remarkable demyelination. Taken together these findings define TNFR1 as crucial mediator in MOG-induced EAE and suggest a protective role for TNFR2 signaling in the clinical course of EAE.

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Documento generato il 27/01/21 alle ore 02:32:46