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  • 2005-2009  (3)
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  • 1
    Electronic Resource
    Electronic Resource
    Epicutaneous exposure to peanut protein prevents oral tolerance and enhances allergic sensitization (2005)
    Oxford, UK : Blackwell Publishing
    Clinical & experimental allergy 35 (2005), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Food allergies are an important cause of life-threatening hypersensitivity reactions. Oral tolerance can be considered the default immune response to dietary antigens, with immune deviation resulting in allergic sensitization. However, primary sensitization to food allergens may not solely be through the gastrointestinal mucosa, as strong T-helper type 2 (Th2)-biased immunity can result from exposure to protein allergens on barrier-disrupted skin.Objective The purpose of this study was to examine whether exposure to allergens through the skin may interfere with the normal development of oral tolerance and promote allergic sensitization to food proteins.Methods Female BALB/c mice were exposed epicutaneously to peanut protein and induction of systemic oral tolerance through high dose feeds of peanut protein was subsequently assessed. Other mice were rendered tolerant prior to epicutaneous peanut exposure. Sensitivity to peanut was determined by assessing delayed-type hypersensitivity, proliferative, cytokine and antibody responses.Results Epicutaneous exposure to peanut protein induced potent Th2-type immunity with high levels of IL-4 and serum IgE. Primary skin exposure prevented the subsequent induction of oral tolerance to peanut in an antigen-specific manner. Upon oral challenge, mice became further sensitized and developed strong peanut-specific IL-4 and IgE responses. Furthermore, animals with existing tolerance to peanut were partly sensitized following epicutaneous exposure.Conclusion Epicutaneous exposure to peanut protein can prevent induction of oral tolerance, and may even modify existing tolerance to peanut. Epidermal exposure to protein allergens selectively drives Th2-type responses, and as such may promote sensitization to food proteins upon gastrointestinal exposure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2005.02260.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Patterns of food allergen-specific cytokine production by T lymphocytes of children with multiple allergies (2005)
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 35 (2005), S. 0 
    Details
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background The contribution of different T cell subsets to the overall measured cytokine response to food allergens is largely unexplored.Method The patterns of cytokine production of peripheral blood-derived T cells after allergen stimulation were studied in 22 children with multiple food allergies and in 20 non-allergic children as controls, using flow cytometry.Results Proportions of T cells of food-sensitized children spontaneously secreting IFN-γ and IL-10 (without antigen stimulation) were lower than non-atopic children and adult controls (P〈inlineGraphic alt="leqslant R: less-than-or-eq, slant" extraInfo="nonStandardEntity" href="urn:x-wiley:09547894:CEA2355:les" location="les.gif"/〉0.001). The proportions of IL-4-producing cells in vitro were significantly increased (P〈inlineGraphic alt="leqslant R: less-than-or-eq, slant" extraInfo="nonStandardEntity" href="urn:x-wiley:09547894:CEA2355:les" location="les.gif"/〉0.04) and IFN-γ-producing cells were significantly reduced (P〈inlineGraphic alt="leqslant R: less-than-or-eq, slant" extraInfo="nonStandardEntity" href="urn:x-wiley:09547894:CEA2355:les" location="les.gif"/〉0.05) in sensitized children after incubation with and without dendritic cell presentation of peanut extract, β-lactoglobulin and ovalbumin. The reverse pattern was found in non-sensitized children and adult controls. IL-4 secretion in allergic children to sensitizing allergens was mainly restricted to the CD4+ CD45 RO+ population while in non-atopic controls both CD4+ and CD8+ CD45 RO+ cells produced mostly IFN-γ. Food-specific IgE values did not correspond with cytokine responses but IL-4 production and IFN-γ reduction relative to normal children were closely associated with total IgE levels.Conclusion Food-allergic children's IL-4 cytokine response to their relevant allergens is predominantly from a memory population of CD4+ CD45 RO+ cells, whereas IL-4 and IFN-γ secretion of non-allergic controls was predominantly from mixed CD4+ and CD8+ CD45 RO+ populations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2222.2005.02355.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    A distinct subset of chemokines dominates the mucosal chemokine response in inflammatory bowel disease (2005)
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 21 (2005), S. 0 
    Details
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background : Inflammatory bowel disease (IBD) is characterised by intense mucosal recruitment of activated leukocytes. Chemokines determine inflammatory leukocyte recruitment and retention.Aim : To compare expression of the entire chemokine family within colonic mucosa from IBD patients and uninflamed controls.Methods : A microarray of cDNAs, representing every member of this superfamily and their cognate receptors, was hybridised with probes derived from colonoscopic biopsies.Results : A distinct subset of chemokines, consisting of CXCLs 1–3 and 8 and CCL20, was upregulated in active colonic IBD, compared with uninflamed areas or tissue from controls. Increased expression of their cognate receptors, CXCR1, CXCR2 and CCR6, was confirmed by quantitative PCR and immunohistochemistry. An identical chemokine response was induced in Caco-2 cells by stimulation with interleukin (IL)-1β, but not tumour necrosis factor-alpha (TNF-α). By contrast, IL-1β and TNF-α were synergistic in an HT29 cell line and primary keratinocytes.Conclusions : IL-1β and TNF-α appear to be the pivotal mediators of a previously unidentified coordinated epithelial chemokine response that dominates the mucosal chemokine environment in inflamed IBD tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2036.2004.02262.x
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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