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  • 1
    Online Resource
    Online Resource
    Basel :S. Karger AG,
    Keywords: Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (203 pages)
    Edition: 1st ed.
    ISBN: 9783318011746
    Series Statement: Chemical Immunology and Allergy Series ; v.86
    Language: English
    Note: Cover -- Contents -- Preface -- Antimicrobial Peptides: Basic Features and Clinical Relevance -- Antimicrobial Peptides in Drosophila: Structures, Activities and Gene Regulation -- Abstract -- Introduction -- Drosophila Defensin, An Anti-Gram-Positive Peptide -- The Antifungal Drosomycin -- Antifungal Peptide -- Metchnikowin, A Cysteine-Free Drosophila Antifungal Peptide -- Cecropins, alpha-Helical Peptides Largely Distributed in Higher Insect Orders -- Drosocin, An Anti-Gram-Negative O-Glycopeptide -- Diptericin, An Anti-Gram-Negative O-Glycopeptide -- Attacins, Large Polypeptides with Antibacterial Properties -- MPAC, the Drosophila Attacin C Pro-Domain with Antibacterial Properties -- Rel Proteins Control Expression of Antimicrobial Peptide Genes -- The Toll and IMD Pathways Control Inducible Expression of AMP Genes -- Other Signaling Pathways Activated during the Drosophila Immune Response -- Hemocytes in the Drosophila Immune Response -- Epithelial Responses in Drosophila -- Concluding Remarks -- Acknowledgements -- References -- Antimicrobial Peptides in Human Skin -- Abstract -- Introduction -- beta-Defensins -- Human beta-Defensin-2 -- Human beta-Defensin-3 -- Human beta-Defensin-1 -- Human beta-Defensin-4 -- Cathelicidin LL-37 -- Serine Protease Inhibitors Antileukoprotease and Elafin -- Dermcidin -- Adrenomedullin -- Neutrophil Gelatinase-Associated Lipocalin -- RNase 7 -- Skin Disease Implications -- Conclusion -- References -- Human Defensins in Crohn's Disease -- Abstract -- Introduction -- Epidemiology: The Role of Hygiene -- Pathophysiology: The Role of Luminal and Mucosal Bacteria -- Defensin Expression and Regulation in the Healthy Intestinal Tract -- Defensins and Inflammatory Bowel Diseases -- NOD2, A Peptidoglycan Receptor and Defensin Expression -- Toll-Like Receptors and Their Expression in Inflammatory Bowel Diseases. , Therapy: The Role of Antibiotics and Probiotics -- Concluding Remarks -- Acknowledgements -- References -- Antimicrobial Peptides in Lung Inflammation -- Abstract -- Introduction -- AMPs Are Expressed in the Respiratory Tract -- Host Defense in the Airways -- AMPs in the Human Lung -- Regulation of the AMPs in the Lung -- Functions of AMPs in the Respiratory Tract -- Antimicrobial Activity -- Inflammation, Angiogenesis, and Cell Function -- Role of AMPs in Pulmonary Disease -- Pneumonia and Tuberculosis -- Cystic Fibrosis and Diffuse Panbronchiolitis -- Asthma and Chronic Obstructive Pulmonary Disease -- Adult Respiratory Distress Syndrome -- Pulmonary Fibrosis and Sarcoidosis -- Conclusions -- Acknowledgement -- References -- Reciprocal Interactions of Host Cells and Microbes -- Bacterial Evasion of Innate Defense at Epithelial Linings -- Abstract -- How to Circumvent Physical Removal from Body Surfaces -- Overcome Space and Nutrient Deprivation -- Resisting the Low-pH Defense Barrier -- Avoid Protease Mediated Destruction and Opsonization -- Evade Recognition and Cell Activation -- Withstand Targeted Destruction -- Active Penetration of the Epithelial Cell Barrier -- Acknowledgements -- References -- Recognition of Bacterial Products by Toll-Like Receptors -- Abstract -- Mammalian Toll-Like Receptors and Their Ligands -- Extracellular Recognition of TLR Ligands -- TLR4 -- TLR2, TLR2/TLR1, and TLR2/TLR6 -- TLR10 -- TLR5 -- TLR11 -- Intracellular Recognition of TLR Ligands -- TLR3 -- TLR7/TLR8 -- TLR9 -- Conclusion -- References -- TLR Signalling and the Function of Dendritic Cells -- Abstract -- Introduction -- What Are Toll-Like Receptors? -- Toll-Like Receptors Recognize Various Molecules -- Signalling Pathway of TLRs -- MyD88-Dependent Pathway -- MyD88-Independent Pathway -- TIRAP/Mal -- TRIF -- TRAM -- The Role of TLR Family in the Host Defence. , TLRs Stimulate DCs to Induce T Cell Activation -- LPS-Stimulated MyD88-Deficient DCs -- DC Subset-Dependent Cytokine Production -- Conclusion -- References -- Contribution of T Cells to Epithelial Defense -- Immunosurveillance by gama/deltaT Cells: Focus on the Murine System -- Abstract -- TCRgamadelta+ Intraepithelial Lymphocytes -- Immunoprotective Roles of gamadelta T Cells in the Tissues -- Immunoregulatory Roles of Local gamadelta T Cells -- gamadelta+ T Cells and Tumor Surveillance -- gamadelta+ T Cell Regulation of Epithelial Malignancy -- From gamadelta Cell Biology in Mice to Immunosurveillance in Humans -- Immunological Mechanisms Highlighted by gamadelta Cells - Towards the Clinic -- References -- gamadelta T Cells Link Innate and Adaptive Immune Responses -- Abstract -- Introduction -- Vgama9/Vdelta2 T Cells -- Vgama9/Vdelta2 T Cells Are Expanded by Various Microbes -- Vgama9/Vdelta2 T Cells Are Activated by Non-Peptide Antigens -- Non-Mevalonate Pathway Intermediates Are the Most Potent Vgama9/Vdelta2 Activators -- Alkylamines Activate Vgama9/Vdelta2 T Cells -- N-Bisphosphonates Stimulate Vgama9/Vdelta2 T Cells -- Vgama9/Vdelta2 T Cells Can Kill Bacteria within Hours after Activation -- The Vgama9/Vdelta2 TCR Repertoire Is Shaped by Non-Peptide Antigens -- Vgama9/Vdelta2 T Cells and Tumor Surveillance -- Activation of Vgama9/Vdelta2 T Cells as a Therapeutic Approach in Tumor Treatment: From Bench to Bedside -- Vdelta1 Cells -- Vdelta1 T Cells Are the Dominant gamma/delta T Cell Population at Mucosal Surfaces -- Vdelta1 T Cells Are Activated by MICA/B -- Vdelta1 T Cells Are Activated by Glycolipids Presented by CD1 -- Lipid Extracts from Gram-Negative Bacteria Indirectly Stimulate Vdelta1T Cells -- TCR Repertoire of Vdelta1 T Cells -- The Role of Vdelta1 T Cells in Microbial Infections -- The Role of Vdelta1 T Cells in Tumor Recognition. , Migration and Homing of gamma/delta T cells -- Chemokine Expression of Peripheral gamma/delta T cells -- gamma/delta T Cells Can Be Polarized into TH1/TH2 Cells -- Chemokine Expression of Mucosal gamma/delta T Cells -- gamma/delta T Cells Can Have Immunosuppressive and Anti-Inflammatory Activities -- Expression of Toll-Like Receptors -- Concluding Remarks -- References -- Author Index -- Subject Index -- A -- B -- C -- D -- E -- F -- G -- H -- I -- L -- M -- N -- P -- R -- S -- T -- Y.
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 82 (2002), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The motor signs of Parkinson's disease have been partly attributed to an overinhibition of the external globus pallidus (GP) that results from hyperactivity of striatopallidal GABA/enkephalinergic neurons. The goals of this study were to measure basal levels of extracellular fluid GABA in the GP of normal cats, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated parkinsonian cats and cats spontaneously recovered from MPTP-induced parkinsonism, and to examine the effects of opioid receptor activation on potassium (K+)-evoked GABA release in the GP in these animals. Basal GP GABA levels were increased 75% from normal in parkinsonian animals 1 week after MPTP administration and returned to control levels in recovered animals 6 weeks afterMPTP administration. No significant differences were observed in K+-evoked GABA release across conditions. The opioid receptor agonist [D-Ala2]-Met-Enkephalinamide (DALA) significantly attenuated K+-evoked GABA release in the GP of MPTP-treated symptomatic and recovered cats, but had no significant effect on GABA release in normal animals. These data show that basal GP GABA levels are elevated coincident with expression of parkinsonian signs and return to normal in animals that have functionally compensated for a nigrostriatal lesion. DALA-induced inhibition of pallidal GABA release after a dopamine-depleting lesion, suggests that enkephalin may attenuate GABA release in the GP specifically after striatal dopamine loss.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 31 (2001), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Desloratadine is a non-sedating, clinically effective, anti-allergic therapy that has been shown to exhibit anti-inflammatory properties that extend beyond its ability to antagonize histamine at H1-receptor sites. This latter effect has been shown in vitro to be both IgE-dependent and -independent.Objective In this study, we addressed the ability of desloratadine to inhibit the in vitro generation of interleukin (IL)-4 and IL-13 from human basophils while concurrently comparing its efficacy in preventing mediator release by these cells.Methods Basophil-enriched suspensions were treated with various concentrations of desloratadine for 15 min before stimulating with either anti-IgE antibody, calcium ionophore, IL-3 or phorbol ester. Histamine (fluorimetry), LTC4 (RIA) and IL-4 (ELISA) were all assayed using the same 4-h culture supernatants. IL-13 (ELISA) was measured in supernatants harvested after 20 h incubation. IL-4 mRNA expression (dilutional RT-PCR) was also examined.Results Desloratadine was found to be nearly six–seven times more potent in preventing the secretion of IL-4 and IL-13 induced by anti-IgE than it was at inhibiting the release of histamine and LTC4. These cytokines were equally inhibited by desloratadine following activation with ionomycin despite the lack of an effect on the histamine induced with ionomycin. Desloratadine had a lesser effect regarding inhibition of the IL-13 secreted in response to IL-3 and PMA. There was no evidence that desloratadine mediated its inhibitory effects by causing decreased cell viability. Finally, IL-4 mRNA accumulation was remarkably inhibited, by as much as 80%, following pretreatment with desloratadine.Conclusion While capable of inhibiting histamine and LTC4 release by human basophils, desloratadine is more effective at targeting the signals regulating IL-4 and IL-13 generation in these cells. This inhibitory effect on cytokine generation provides additional evidence that this antihistamine exerts anti-inflammatory properties.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background The complex interactions between immune cells are partly mediated by different adhesion molecules, but little is known about their role in the systemic immunoinflammatory process following sensitization to food antigens in early infancy.Objective The aim of this study was to investigate the expression of intercellular adhesion molecule-1 (ICAM-1or CD54) and the α subunits of its ligands' lymphocyte function-associated antigen-1 (LFA-1) (αL subunit or CD11a) and Mac-1 (αM subunit or CD11b) on peripheral blood leucocytes in infants with cow's milk allergy (CMA) and in healthy controls.Methods Thirty-nine breastfed infants, aged from 0.6 to 8.3 months, and their lactating mothers were included in the study from delivery onwards. During follow-up, 25 infants developed CMA and 14 remained healthy. Expressions of CD54 and CD11b on peripheral blood leucocytes were evaluated by flow cytometry. In addition, the expression of CD11a on peripheral blood leucocytes was analysed by immunocytochemistry. Mothers' milk samples were collected and their leucocyte content was evaluated using a light microscope.Results The frequency of ICAM-1 expressing peripheral blood lymphocytes was significantly higher in patients with CMA than in healthy infants (P=0.03, Mann–Whitney U-test). Furthermore, the high proportion of ICAM-1-expressing cells was associated with gastrointestinal and multiorgan symptoms in the CMA infants. There was no significant difference in the expression of Mac-1 αM on lymphocytes in our study groups, but the LFA-1 αL expression seemed to be higher in the IgE-mediated CMA.Conclusion We suggest that the high expression of ICAM-1 on peripheral blood lymphocytes may reflect enhanced stimulation of T cells in vivo and their migration to the effector tissues in an early-phase of developing CMA. Furthermore, high ICAM-1 expression may be associated with the presence of multiorgan manifestations of CMA, whereas high LFA-1 expression may reflect the IgE-mediated disease.
    Type of Medium: Electronic Resource
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