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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
    Publication Date: 2016-03-11
    Description: Evidence shows that factor VIII (FVIII) ectopically expressed in platelets (2bF8) is therapeutic in FVIII null mice even with anti-FVIII inhibitory antibodies (inhibitors). If current efforts to generate platelets in vitro succeed, genetically manipulated platelets containing FVIII may be used therapeutically in hemophilia A patients with inhibitors. One important concern is the immunogenicity of platelet-derived FVIII. To address this concern, we infused 2bF8 transgenic (2bF8 Tg ) platelets into naïve FVIII null mice weekly for 8 weeks. No anti-FVIII antibodies were detected in the infused animals during the study course. We then explored whether platelet-derived FVIII is immunogenic in FVIII null mice with inhibitors. The 2bF8 Tg platelets were transfused into rhF8-primed FVIII null mice, resulting in no augmentation of anti-FVIII antibodies. To investigate whether preconditioning affects the immune response, animals were sublethally irradiated and subsequently transfused with 2bF8 Tg platelets. No anti-FVIII antibodies were detected in the recipients after platelet infusions. Following further challenge with rhF8, the inhibitor titer in this group was significantly lower than in naïve FVIII null mice utilizing the same immunization protocol. Thus, our data demonstrate that infusion of platelets containing FVIII triggers neither primary nor memory anti-FVIII immune response in FVIII null mice and that sublethal irradiation plus 2bF8 Tg platelet infusion suppresses anti-FVIII immune response in FVIII null mice.
    Keywords: Thrombosis and Hemostasis
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 3
    Publication Date: 2014-01-17
    Description: Our previous studies have demonstrated that platelet FVIII (2bF8) gene therapy can improve hemostasis in hemophilia A mice, even in the presence of inhibitory antibodies, but none of our studies has targeted human cells. Here, we evaluated the feasibility for lentivirus (LV)-mediated human platelet gene therapy of hemophilia A. Human platelet FVIII expression was introduced by 2bF8LV-mediated transduction of human cord blood (hCB) CD34 + cells followed by xenotransplantation into immunocompromised NSG mice or NSG mice in an FVIII null background (NSGF8KO). Platelet FVIII was detected in all recipients that received 2bF8LV-transduced hCB cells as long as human platelet chimerism persisted. All NSGF8KO recipients (n = 7) that received 2bF8LV-transduced hCB cells survived tail clipping if animals had greater than 2% of platelets derived from 2bF8LV-transduced hCB cells, whereas 5 of 7 survived when human platelets were 0.3% to 2%. Whole blood clotting time analysis confirmed that hemostasis was improved in NSGF8KO mice that received 2bF8LV-transduced hCB cells. We demonstrate, for the first time, the feasibility of 2bF8LV gene delivery to human hematopoietic stem cells to introduce FVIII expression in human platelets and that human platelet–derived FVIII can improve hemostasis in hemophilia A.
    Keywords: Thrombosis and Hemostasis, Gene Therapy
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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