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  • 1
    Online Resource
    Online Resource
    San Diego :Elsevier Science & Technology,
    Keywords: Transgenic mice. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (339 pages)
    Edition: 1st ed.
    ISBN: 9781483296494
    Language: English
    Note: Front Cover -- Transgenesis and Targeted Mutagenesis in Immunology -- Copyright Page -- Table of Contents -- Contributors -- Preface -- Chapter 1. Transgenic Mouse Models to Study VDJ Recombination -- I. Introduction -- II. Transgenic Model to Define VDJ Recombination Regulatory Elements: Evidence That Recombinational Sequences Are Associated with Lymphoid Transcriptional Enhancers -- III. Other Transgenic Models -- IV. Future Prospects -- V. Concluding Remarks -- Acknowledgments -- References -- Chapter 2. Lymphocyte Development and Function in T Cell Receptor and RAG-1Mutant Mice -- I. Introduction -- II. Creation of Mutant Mice -- III. Thymocyte Development -- IV. Model for the Role of TCR Genes in αß Thymocyte Differentiation -- V. Lymphocyte Function -- Acknowledgments -- References -- Chapter 3. RAG-2-Deficient Blastocyst Complementation -- I. Introduction -- II. Procedures -- III. Applications -- IV. Prospects -- Acknowledgments -- References -- Chapter 4. Role of CD4 and CD8 in Determining Cell Fate in the Thymus -- I. Background -- II. Coreceptor Transgenes and TCR Repertoire Selection -- III. Coreceptor Transgenes and Thymocyte Lineage Commitment -- IV. Other Data Pertaining to Coreceptor Lineage Commitment -- V. Future Directions -- Acknowledgments -- References -- Chapter 5. T Cell Development in CD4, CD8, and p56ICK Gene-Targeted Mice -- I. Introduction -- II. T Cell Development in CD4, CD8, and CD4 and CD8 Double-Negative Mice -- III. Thymic Development in p56ICK-Deficient Mice -- IV. Concluding Remarks -- References -- Chapter 6. T Cell Tolerance in T Cell Receptor Transgenic Ipr/lpr Mice -- I. Introduction -- II. Effect of T Cell Receptor Transgenes on T Cell Development in Ipr/lpr Mice -- III. Loss of T Cell Tolerance in Db/HY T Cell Receptor Transgenic Ipr/lpr Mice. , IV. Loss of T Cell Tolerance in Vβ8 T Cell Receptor Transgenic MRL Ipr/lpr Mice Neonatally Tolerized by the Staphylococcal Enterotoxin B -- V. Costimulatory Signaling in Vβ8 T Cell Receptor Transgenic MRL Ipr/lpr Mice Neonatally Tolerized with Staphylococcal Enterotoxin B -- VI. Summary -- Acknowledgments -- References -- Chapter 7. Thymocyte Selection and Peripheral Tolerance Using the Lymphocytic Choriomeningitis Virus as a Model Antigen -- I. Introduction -- II. Positive Selection -- III. Negative Selection -- IV. Tolerance to Peripheral Self-Antigens -- V. Factors That Influence the Induction of Self-Reactivity -- VI. Prevention of Autoimmune Disease -- VII. Concluding Remarks -- Acknowledgments -- References -- Chapter 8. Peripheral T Cell Tolerance: Distinct Levels and Multistep Mechanisms -- I. Introduction -- II. Thymic Tolerance Induction by Minute Amounts of Antigen -- III. Parameters Controlling Peripheral Tolerance Induction -- IV. Distinct Manifestations of Peripheral Tolerance Due to Differential Expression of Self-Antigen -- V. Influence of the Amount of Antigen Expressed on Peripheral Tolerance Induction -- VI. Tolerance Induction as a Multistep Process -- VII. Anergy versus Memory -- VIII. Summary and Conclusions -- References -- Chapter 9. Peripheral Tolerance and CD4+ T Cells -- I. Introduction -- II. Class II MHC Transgenic Animals -- III. INS-HA Transgenic Animals -- IV. TCR INS-HA Transgenic Animals -- V. Discussion -- VI. Conclusions -- Acknowledgments -- References -- Chapter 10. Studies of Tolerance, Inflammation, and Autoimmunity inTransgenic Mice -- I. Introduction -- II. TNFα and TNFβ Are Sufficient to Induce an Inflammatory Infiltrate but Cannot Induce Autoimmunity -- III. Antigen Recognition and Its Consequences in SV-40 T Antigen Transgenic Mice. , IV. Two-Signal Model of T Cell Activation: Role of T Cell Activation in the Induction of Autoimmunity -- V. Can Locally Produced Interleukin 2 Bypass Tolerance Mechanisms?: Interleukin 2 Expression in Pancreatic B Cells Leads to Insulitis and Diabetes -- VI. Concluding Remarks -- Acknowledgments -- References -- Chapter 11. Immunological Studies Utilizing Cytokine Transgenic Mice -- I. Introduction -- II. Localized Expression of Interferon y -- III. Expression of Interleukin 10, an Immunoinhibitory Cytokine -- IV. Expression of Other Cytokines -- V. Expression of Molecules Other Than Cytokines -- VI. Conclusion -- References -- Chapter 12. Effect of MHC Class II Encoding Transgenes on Autoimmunity in Nonobese Diabetic Mice -- I. Introduction -- II. Effect of Transgenic Ea Expression on Insulin-Dependent Diabetes Mellitus -- III. Effect of Mutated Ab Transgenes on Insulin-Dependent Diabetes Mellitus -- IV. Conclusion -- References -- Chapter 13. Development and Function of the Immune System in Mice with Targeted Disruption of the Interleukin 2 Gene -- I. Introduction -- II. Generation of Interleukin 4-Deficient Mice by Targeted Mutagenesis -- III. Effect of Interleukin 4 on B Cell Development and Differentiation -- IV. Effect of Interleukin 4 on T Cell Development and Differentiation -- V. Role of Interleukin 4 in Allergy -- VI. Outlook -- Acknowledgments -- References -- Chapter 14. Immune Responses in Interleukin 4-Deficient Mice -- I. Introduction -- II. Generation of Interleukin 2-Deficient Mice -- III. Lymphopoiesis and Leukocyte Homeostasis in Young and Adult Mutant Mice -- IV. Immune Functions in Young Healthy Animals -- V. Development of Disease and Mortality of Adult Interleukin 2-Deficient Mice -- VI. Inflammatory Bowel Disease in Interleukin 2-Deficient Mice -- VII. Concluding Remarks -- References. , Chapter 15. Manipulation of Transgene-Encoded Self-Antigens to Explore Mechanisms of B Cell Tolerance -- I. Introduction -- II. Anti-CD8 IgM Transgenic Mouse Lines -- III. Conclusions -- Acknowledgments -- References -- Chapter 16. Transgenic Mouse Model for Peripheral B Cell Tolerance -- I. Introduction -- II. Effects of Lysozyme on Self-Reactive B Cells -- III. B Cell Anergy versus Elimination -- IV. Physiological and Pathological Implications of B Cell Elimination by Arrested Development -- References -- Chapter 17. Immunobiology of MHC Class l-Deficient Mice -- I. Introduction -- II. Production of ß2m-Deficient Mice -- III. Effects of ß2m Deficiency on Cell Surface Expression of Class I Molecules -- IV. Defective Lymphocyte Development in Class l-Deficient Mice -- V. Effect of Class I Deficiency on Susceptibility to Natural Killer Cells and Development of Natural Killer Activity -- VI. Transplantation Studies -- VII. Responses of Class l-Deficient Mice to Pathogens -- VIII. Summary and Conclusions -- Acknowledgments -- References -- Chapter 18. MHC Class II Mutant Mice -- I. Introduction -- II. Studies in MHC Class II Mutant Mice -- III. MHC-Deficient Mice -- IV. Conclusion -- Acknowledgments -- References -- Index.
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  • 2
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Tight junctions form the diffusion barrier of brain microcapillary endothelial cells and support cell polarity. Also astrocytes express tight junction components such as occludin, claudin-1, ZO-1 and ZO-2, but do not establish a permeability barrier. However, little is known about the function and regulation of these molecules in astrocytes. We studied the impact of tumour necrosis factor (TNF) on occludin and ZO-1 expression in astrocytes. TNF decreased occludin, but not ZO-1 expression. In brain microcapillary endothelial cells, as well as in epithelial cells, occludin expression was not influenced by TNF. Removal of TNF from astrocytes restored the basal level of occludin. Down-regulation was inhibited by caffeic acid phenethyl ester, a specific inhibitor of nuclear factor-κB (NF-κB) activation. Exposure of astrocytes isolated from mice deficient in either TNF type-1 receptor (TNFR1), TNF type-2 receptor (TNFR2), or both, respectively, revealed that down-regulation was mediated entirely by TNFR1. ZO-1, which can interact with occludin, was found to co-precipitate connexin43, but not occludin. These findings demonstrate that TNF selectively down-regulates occludin in astrocytes, but not in cells forming established tight junctions, through TNFR1 and suggest that NF-κB is involved as a negative regulator.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 546 (1988), 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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  • 4
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Nerve injury triggers numerous changes in the injured neurons and surrounding non-neuronal cells. Of particular interest are molecular signals that play a role in the overall orchestration of this multifaceted cellular response. Here we investigated the function of interleukin-6 (IL6), a multifunctional neurotrophin and cytokine rapidly expressed in the injured nervous system, using the facial axotomy model in IL6-deficient mice and wild-type controls. Transgenic deletion of IL6 caused a massive decrease in the recruitment of CD3-positive T-lymphocytes and early microglial activation during the first 4 days after injury in the axotomized facial nucleus. This was accompanied by a more moderate reduction in peripheral regeneration at day 4, lymphocyte recruitment (day 14) and enhanced perikaryal sprouting (day 14). Motoneuron cell death, phagocytosis by microglial cells and recruitment of granulocytes and macrophages into injured peripheral nerve were not affected. In summary, IL6 lead to a variety of effects on the cellular response to neural trauma. However, the particularly strong actions on lymphocytes and microglia suggest that this cytokine plays a central role in the initiation of immune surveillance in the injured central nervous system.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature medicine 1 (1995), S. 437-441 
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] For B cells to make antibodies against most antigens, they require help from T cells. T cell help is delivered as two signals to the B cell, one of which is via CD40 and the other can be through receptors for any of a variety of soluble cytokines. We have constructed recombinant vaccinia viruses ...
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1546-1696
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: [Auszug] Tetracycline-regulated gene expression in eukaryotic cell lines, plants, and transgenic mice has become a powerful tool for the analysis of eukaryotic gene expression and function. The system consists of two plasmids, one encoding the transactivator protein under control of a viral cytomegalovirus ...
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The thymus is organized into medullary and cortical zones that support distinct stages of T-cell development. The formation of medulla and cortex compartments is thought to occur through invagination of an endodermal epithelial sheet into an ectodermal one at the third pharyngeal pouch and ...
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Although prion proteins are most efficiently propagated through intracerebral inoculation, peripheral administration has caused the diseases kuru, iatrogenic Creutzfeldt–Jakob disease (CJD), bovine spongiform encephalopathy (BSE) and new-variant CJD,. The development of neurological ...
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Interleukin-4 has been reported to critically modulate Borrelia burgdorferi infection and Lyme arthritis in experimental murine models. To determine the in vivo role of IL-4 in controlling Lyme carditis, we compared immunological responses and the severity of cardiac inflammation in wild-type BALB/c (IL-4 +/+) and IL-4 deficient BALB/c (IL-4 −/−) mice infected with B. burgdorferi by tick-bite. At day 15 and 30 post-infection IL-4 −/− mice produced significantly greater titers of spirochete-specific IgG2a than the wild-type IL-4 +/+ mice, which produced significantly more spirochete-specific IgG1. Following in vitro antigenic stimulation with B. burgdorferi antigen, splenocytes from infected IL-4 −/− and IL-4 +/+ mice displayed similar magnitudes of proliferative responses at day 15 and 30 post-infection. At day 30 antigen-stimulated splenocytes from infected IL-4 −/− mice, however, produced significantly more IFN-γ than those derived from similarly infected IL-4 +/+ mice, suggesting that Th1-influenced responses predominated in IL-4 −/− mice. Moreover, inflamed hearts from IL-4 −/− mice displayed higher levels of IFN-γ and TNF-α transcripts as compared to IL-4 +/+ mice. At both time points antigen-stimulated splenocytes from IL-4 +/+ and IL-4 −/− mice produced significant amounts of IL-10 but those from IL-4 +/+ mice produced either no or little IL-4. Histopathology demonstrated typical Lyme carditis in both IL-4 +/+ and IL-4 −/− mice at day 15 and day 30. Although Borrelia-infected IL-4 −/− mice developed a more severe carditis on day 30, the carditis resolved by day 50, as it did in IL4 +/+ mice. These results indicate that although IL-4 may help limit the severity of Lyme carditis, its absence does not preclude resolution of cardiac lesions.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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