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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 771 (1995), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract The signalling mechanisms that regulate epidermal permeability barrier homeostasis arc not known. Previous Northern blot analysis showed that both acute and chronic barrier disruption increase mRNA levels of several cytokines in murine epidermis. To further characterize the epidermal response to barrier abrogation, we used more sensitive, multi-probe RNasc protection assays to measure the mRNA levels of additional cytokines. as well as cytokine receptors in acute and chronic models of barrier disruption. Normal mouse epidermis expressed interleukin (IL)-lα, interferon-γ (IFN-γ). tumor necrosis factor-α (TNF-α) and IL-6 mRNAs. Following tape-stripping, only the mRNA levels for TNF-α, IL-lα, IL-lβ and IL-6 increased at 2.5 and 7 h, and returned toward normal levels by IX h. No mRNAs encoding TNF-β. IL-2, IL-3. IL-4 or IL-5, were detected in the epidermis either under basal conditions or after tape-stripping. Similarly, in a chronic model, essential fatty acid deficiency, epidermal levels of TNF-α, IL-lα, IL-lβ and IL-6 mRNAs, but not IFN-γ mRNA. were elevated over controls; and again, mRNAs for the remaining probed cytokines were not detected. In contrast, in the dermis. only IL-Iβ mRNA levels increased 2.5 h after tape-stripping, and remained elevated at I8 h. mRNAs encoding the IL-1 (p60), IFN-γ ami IL-6 receptors were present in epidermis, but their levels remained unchanged following either acute or chronic barrier disruption. In contrast, epidermal TNF (p55) receptor mRNA levels were increased by 87% (P〈0.01) at 2.5 h, returned to control levels at 7 h and were increased by 68% (p〈0.03) at 18 h after tape-stripping. The increase at 2 h was confirmed by Northern blot analysis and was not prevented by latex occlusion performed immediately after tape-stripping. mRNAs for the IL-I (p80) receptor and TNF (p75) receptor were not detected in epidermis. Low levels of TNF (p55) receptor mRNA were present in the dermis. and they remained unchanged after tape-stripping. The presence of specific receptor mRNAs in the epidermis and dermis suggests that these tissues are capable of responding in an autocrine and/or paracrine fashion to the cognate cytokines. These results suggest that epidermal cytokines produced after barrier disruption may initiate a cytokine cascade which could regulate cytokine and cytokine receptor production and/or inflammatory responses.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Key words Reactive astrocytes ; Central nervous ; system ; Immunocytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Astrocytes respond vigorously to diverse neurological insults. It is still not clear, however, whether this response is stereotypic following different insults or varies according to the injury. We have used a novel immunocytochemical marker of reactive astrocytes, termed M22, together with antibodies to glial fibrillary acidic protein (GFAP), to analyze region- and insult-specific differences in reactive astrocytosis in the murine central nervous system (CNS). Pathology was variously induced by (1) infectious agents, (2) transgenic overexpression of a viral glycoprotein or cytokine, or (3) focal trauma. Scrapie infection induced high levels of both GFAP and M22 epitope expression by hippocampal reactive astrocytes, but neither scrapie nor wild mouse retrovirus infection induced detectable M22 staining in reactive astrocytes of the caudal brain. Focal trauma and human immunodeficiency virus gp120 overexpression induced M22 expression only in the hippocampus, while interleukin-6 overexpression induced it in cerebellar astrocytes. Although M22 expression was limited to areas with extensive damage, GFAP expression was induced in every region of the mouse brain displaying pathology. Staining of routinely fixed human brain tissue demonstrated that M22 also labeled reactive astrocytes in chronic human CNS disease. The restriction of M22 expression to areas of strongly GFAP-positive astrocytosis suggests that the M22 antibody identified highly activated reactive astrocytes. Because of this selective staining of activated astrocytes, the M22 antibody may provide neuropathologists with a good marker for qualitative analysis of the astrocytic response to different injuries.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1573-4935
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 40 (1989), S. 57-66 
    ISSN: 0730-2312
    Keywords: IFN- and TNF-pancreatic beta cell function ; insulin secretion and content ; effects of IFN- and TNF-reovirus infection ; major histocompatibility complex protein expression ; RIN-m5F cells major histocompatibility complex protein expression ; major histocompatibility complex ; mRNA levels ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Insulin-dependent (type 1) diabetes mellitus (IDDM) is due to the selective autoimmune-mediated destruction of pancreatic beta cells possibly initiated by viruses. To elucidate the possible role of viruses and cytokines in the pathogenesis of IDDM, we have examined the effect of reovirus infection on beta cell major histocompatibility complex (MHC) expression and the effect of interferon-γ (IFN-γ) and tumour necrosis factor-α (TNF-α) on beta cell function in vitro. Infection of RIN-m5F (rat insulinoma) cells with reovirus-1 or reovirus-3 was associated with a tenfold increase in class 1 MHC protein and mRNA expression. Reovirus infection did not induce the expression of class 11 MHC by RIN-m5F cells. Exposure of reovirus to ultraviolet light almost completely abolished its ability to induce class 1 MHC protein expression on infected cells.Murine islets cultured for 3 days with IFN-γ and/or TNF-α had a significantly reduced insulin response to glucose, which was more marked with a combination of the cytokines. During 6 days of culture in IFN-γ plus TNF-α islets underwent noticeable degeneration associated with an 80% reduction in insulin content. These findings together with previous data suggest viruses and cytokines may have multiple roles in beta cell destruction, indirectly through enhanced MHC protein expression and directly through functional impairment and loss of viability.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
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