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Titolo:
Superantigen overcomes resistance of IL-6-deficient mice towards MOG-induced EAE by a TNFR1 controlled pathway
Autore:
Eugster, HP; Frei, K; Winkler, F; Koedel, U; Pfister, W; Lassmann, H; Fontana, A;
Indirizzi:
Univ Zurich Hosp, Dept Internal Med, Clin Immunol Sect, CH-8044 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8044 CH-8044 Zurich, Switzerland Univ Zurich Hosp, Dept Neurosurg, CH-8091 Zurich, Switzerland Univ Zurich Hosp Zurich Switzerland CH-8091 CH-8091 Zurich, Switzerland Univ Munich, Klinikum Grosshadern, D-8000 Munich, Germany Univ Munich Munich Germany D-8000 um Grosshadern, D-8000 Munich, Germany Univ Vienna, Inst Neurol, Vienna, Austria Univ Vienna Vienna AustriaUniv Vienna, Inst Neurol, Vienna, Austria
Titolo Testata:
EUROPEAN JOURNAL OF IMMUNOLOGY
fascicolo: 8, volume: 31, anno: 2001,
pagine: 2302 - 2312
SICI:
0014-2980(200108)31:8<2302:SOROIM>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; MYELIN OLIGODENDROCYTE GLYCOPROTEIN; TUMOR-NECROSIS-FACTOR; STAPHYLOCOCCAL ENTEROTOXIN-B; CENTRAL-NERVOUS-SYSTEM; T-CELLS; COMPLEMENT COMPONENT; H-2(B) MICE; IN-VIVO;
Keywords:
superantigen; EAE; IL-6; myelin oligodendrocyte glycoprotein; neutrophil;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Fontana, A Univ Zurich Hosp, Dept Internal Med, Clin Immunol Sect, Haeldeliweg 4, CH-8044 Zurich, Switzerland Univ Zurich Hosp Haeldeliweg 4 Zurich Switzerland CH-8044 land
Citazione:
H.P. Eugster et al., "Superantigen overcomes resistance of IL-6-deficient mice towards MOG-induced EAE by a TNFR1 controlled pathway", EUR J IMMUN, 31(8), 2001, pp. 2302-2312

Abstract

Experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein peptide 35-55 (MOG) leads to a chronic form of diseasecharacterized by demyelination, inflammation and gliosis in the central nervous system (CNS). Recently IL-6 and LT alpha were found to be required for induction of the disease. The main features associated with EAE resistance of IL-6(-/-) and LT alpha (-/-) mice were reduced T cell proliferation and endothelial activation. As shown here treatment of MOG-immunized IL-6(-/-) mice with staphylococcal enterotoxin B (SEB) reversed their resistance toMOG-induced EAE. SEB failed to restore susceptibility to EAE in LT alpha (-/-) mice. The effect of SEB to induce EAE in IL-6(-/-) mice depends on TNFreceptor type 1 (TNFR1) signaling because IL-6/TNF/LT alpha (-/-) and IL-6/TNFR1(-/-) are refractory to SEB. TNFR1 is involved in SEB induced trafficking of T cells into the CNS as evidenced by the failure to up-regulate VCAM-1 on CNS endothelium and lack of accumulation of V beta8(+) T cells in the CNS of IL-6/TNFR1(-/-) mice upon immunization with MOG and treatment withSEB. The course of SEB triggered EAE in MOG immunized IL-6(-/-) mice was characterized by reduced severity and duration of clinical manifestations, which were associated with a significant drop of CNS infiltrating neutrophils and MIP-2 expression after peak disease. Taken collectively the effect ofSEB to overcome EAE resistance points to a transient IL-6 independent but TNFR1 dependent proinflamatory pathway in EAE pathogenesis and suggests a crucial function for IL-6 in disease perpetuation.

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Documento generato il 27/01/21 alle ore 02:39:16