Neutrophils secreting tumor necrosis factor alpha infiltrate the central nervous system of BALB/c mice with experimental autoimmune encephalomyelitis
Identifieur interne : 001259 ( Istex/Checkpoint ); précédent : 001258; suivant : 001260Neutrophils secreting tumor necrosis factor alpha infiltrate the central nervous system of BALB/c mice with experimental autoimmune encephalomyelitis
Auteurs : Jorma A. M Tt [Finlande] ; Ulrika R. Sjöholm [Finlande] ; Petra T. Nyg Rdas [Finlande] ; Aimo A. Salmi [Finlande] ; Ari E. Hinkkanen [Finlande]Source :
- Journal of Neuroimmunology [ 0165-5728 ] ; 1998.
English descriptors
- Teeft :
- Active stage, Adjuvant, Autoimmune, Autoimmune encephalomyelitis, Balbrc, Balbrc mice, Balbrc mice immunised, Balbrc mouse, Boehringer mannheim, Cd4q, Cellular infiltrates, Chemokine, Chemokine mrnas, Cytokine, Dendritic, Dendritic cells, Encephalomyelitis, Harlan laboratories, Immune, Immune cells, Immune response, Immunisation, Immunisation groups, Immunised, Immunised balbrc mice, Immunised balbrc mouse, Immunised mice, Immunised mouse, Immunol, Infiltrates, Lewis rats, Maatta, Macrophage, Medulla, Medulla oblongata, Microglia, Monocyte, Mouse, Mrna, Mrna expression, Murine, Myelin antigens, Neuroimmunol, Neuroimmunology, Neutrophil, Oblongata, Owens, Popliteal lymph nodes, Positive cells, Reaction mixture, Same region, Spinal, Spinal cord, Subarachnoidal, Successive coronal sections, Tumor necrosis factor, Turku.
Abstract
Abstract: Experimental autoimmune encephalomyelitis (EAE) can be induced in resistant BALB/c mice by ultrasound-formed adjuvant emulsion. In contrast to susceptible mouse strains large numbers of neutrophils secreting TNF-α occupied the central nervous system (CNS) of BALB/c mice with severe EAE, whereas only small numbers of macrophages and CD4+ T-cells could be detected. CNS infiltration was preceded with activation of microglial cells. Ultrasound formed adjuvant induced early IFN-γ expression in popliteal lymph nodes of BALB/c mice, whereas conventional adjuvant induced delayed IFN-γ production. Although the clinical outcome of EAE was similar to that seen in susceptible mice, the pathogenesis was distinct having possible implications on the different forms seen in multiple sclerosis.
Url:
DOI: 10.1016/S0165-5728(98)00135-0
Affiliations:
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Hinkkanen</name><affiliation wicri:level="1"><country xml:lang="fr">Finlande</country><wicri:regionArea>Turku Immunology Centre and Department of Biochemistry and Pharmacy, Åbo Akademi University, P.O. Box 66, FIN-20521 Turku</wicri:regionArea><wicri:noRegion>FIN-20521 Turku</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neuroimmunology</title><title level="j" type="abbrev">JNI</title><idno type="ISSN">0165-5728</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1998">1998</date><biblScope unit="volume">90</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="162">162</biblScope><biblScope unit="page" to="175">175</biblScope></imprint><idno type="ISSN">0165-5728</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0165-5728</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Active stage</term><term>Adjuvant</term><term>Autoimmune</term><term>Autoimmune encephalomyelitis</term><term>Balbrc</term><term>Balbrc mice</term><term>Balbrc mice immunised</term><term>Balbrc mouse</term><term>Boehringer mannheim</term><term>Cd4q</term><term>Cellular infiltrates</term><term>Chemokine</term><term>Chemokine mrnas</term><term>Cytokine</term><term>Dendritic</term><term>Dendritic cells</term><term>Encephalomyelitis</term><term>Harlan laboratories</term><term>Immune</term><term>Immune cells</term><term>Immune response</term><term>Immunisation</term><term>Immunisation groups</term><term>Immunised</term><term>Immunised balbrc mice</term><term>Immunised balbrc mouse</term><term>Immunised mice</term><term>Immunised mouse</term><term>Immunol</term><term>Infiltrates</term><term>Lewis rats</term><term>Maatta</term><term>Macrophage</term><term>Medulla</term><term>Medulla oblongata</term><term>Microglia</term><term>Monocyte</term><term>Mouse</term><term>Mrna</term><term>Mrna expression</term><term>Murine</term><term>Myelin antigens</term><term>Neuroimmunol</term><term>Neuroimmunology</term><term>Neutrophil</term><term>Oblongata</term><term>Owens</term><term>Popliteal lymph nodes</term><term>Positive cells</term><term>Reaction mixture</term><term>Same region</term><term>Spinal</term><term>Spinal cord</term><term>Subarachnoidal</term><term>Successive coronal sections</term><term>Tumor necrosis factor</term><term>Turku</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Experimental autoimmune encephalomyelitis (EAE) can be induced in resistant BALB/c mice by ultrasound-formed adjuvant emulsion. In contrast to susceptible mouse strains large numbers of neutrophils secreting TNF-α occupied the central nervous system (CNS) of BALB/c mice with severe EAE, whereas only small numbers of macrophages and CD4+ T-cells could be detected. CNS infiltration was preceded with activation of microglial cells. Ultrasound formed adjuvant induced early IFN-γ expression in popliteal lymph nodes of BALB/c mice, whereas conventional adjuvant induced delayed IFN-γ production. 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Salmi</name><name sortKey="Sjoholm, Ulrika R" sort="Sjoholm, Ulrika R" uniqKey="Sjoholm U" first="Ulrika R." last="Sjöholm">Ulrika R. Sjöholm</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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