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  • 1
    Electronic Resource
    Electronic Resource
    JNK3 contributes to c-Jun activation and apoptosis but not oxidative stress in nerve growth factor-deprived sympathetic neurons (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 78 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The stress activated protein kinase pathway culminates in c-Jun phosphorylation mediated by the Jun Kinases (JNKs). The role of the JNK pathway in sympathetic neuronal death is unclear in that apoptosis is not inhibited by a dominant negative protein of one JNK kinase, SEK1, but is inhibited by CEP-1347, a compound known to inhibit this overall pathway but not JNKs per se. To evaluate directly the apoptotic role of the JNK isoform that is selectively expressed in neurons, JNK3, we isolated sympathetic neurons from JNK3-deficient mice and quantified nerve growth factor (NGF) deprivation-induced neuronal death, oxidative stress, c-Jun phosphorylation, and c-jun induction. Here, we report that oxidative stress in neurons from JNK3-deficient mice is normal after NGF deprivation. In contrast, NGF-deprivation-induced increases in the levels of phosphorylated c-Jun, c-jun, and apoptosis are each inhibited in JNK3-deficient mice. Overall, these results indicate that JNK3 plays a critical role in activation of c-Jun and apoptosis in a classic model of cell-autonomous programmed neuron death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00400.x
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  • 2
    Electronic Resource
    Electronic Resource
    Walking through the forest of transgenic models of human disease (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 169 (1999), S. 0 
    Details
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: In the investigation of human disease, molecular biology has provided Immunologists with several enormously powerful tools. Trans-genic and knockout mice provide animal models to investigate mechanisms, as well as aid in the design of therapies for these diseases. These mice have been useful in several different ways. First, as direct models of disease they provide direct tools for the study of the disease. Second, expression of individual molecules can be altered in the context of established disease models. We describe here some of the models in use as well as the limitations and promise of this research.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-065X.1999.tb01301.x
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  • 3
    Electronic Resource
    Electronic Resource
    CD40 AND CD154 IN CELL-MEDIATED IMMUNITY (1998)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Immunology 16 (1998), S. 111-135 
    Details
    ISSN: 0732-0582
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology , Medicine
    Notes: Abstract CD40-CD154-mediated contact-dependent signals between B and T cells are required for the generation of thymus dependent (TD) humoral immune responses. CD40-CD154 interactions are however also important in many other cell systems. CD40 is expressed by a large variety of cell types other than B cells, and these include dendritic cells, follicular dendritic cells, monocytes, macrophages, mast cells, fibroblasts, and endothelial cells. CD40- and CD154-knockout mice and antibodies to CD40 and CD154 have helped to elucidate the role of the CD40-CD154 system in immune responses. Recently published studies indicate that CD40-CD154 interactions can influence T cell priming and T cell-mediated effector functions; they can also upregulate costimulatory molecules and activate macrophages, NK cells, and endothelia as well as participate in organ-specific autoimmune disease, graft rejection, and even atherosclerosis. This review focuses on the role of the CD40-CD154 system in the regulation of many newly discovered functions important in inflammation and cell-mediated immunity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.immunol.16.1.111
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  • 4
    Electronic Resource
    Electronic Resource
    MAP KINASES IN THE IMMUNE RESPONSE (2002)
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Immunology 20 (2002), S. 55-72 
    Details
    ISSN: 0732-0582
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology , Medicine
    Notes: Abstract MAP kinases are among the most ancient signal transduction pathways and are widely used throughout evolution in many physiological processes. In mammalian species, MAP kinases are involved in all aspects of immune responses, from the initiation phase of innate immunity, to activation of adaptive immunity, and to cell death when immune function is complete. In this review, we summarize recent progress in understanding the function and regulation of MAP kinase pathways in these phases of immune responses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1146/annurev.immunol.20.091301.131133
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  • 5
    Electronic Resource
    Electronic Resource
    Specific pathophysiological functions of JNK isoforms in the brain (2005)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 21 (2005), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have investigated the effect of JNK1 ko, JNK2 ko, JNK3 ko, JNK2+3 ko and c-JunAA mutation on neuronal survival in adult transgenic mice following ischemia, 6-hydroxydopamine induced neurotoxicity, axon transection and kainic acid induced excitotoxicity. Deletion of JNK isoforms indicated the compartment-specific expression of JNK isoforms with 46-kDa JNK1 as the main phosphorylated JNK isoform. Permanent occlusion of the MCA significantly enlarged the infarct area in JNK1 ko, which showed an increased expression of JNK3 in the penumbra. Survival of dopaminergic neurons in the substantia nigra compacta (SNC) following intrastriatal injection of 6-hydroxydopamine was transiently improved in JNK3 ko and c-JunAA mice after 7 days, but not 60 days. Following transection of the medial forebrain bundle, however, JNK3 ko conferred persisting neuroprotection of axotomised SNC neurons. None of the JNK ko and c-JunAA mutation affected the survival of facial motoneurons following peripheral axotomy when investigated after 90 days. Finally, we determined the impact of JNK ko on the survival of animals and the degeneration of hippocampal neurons following kainic acid. JNK3 ko mice were substantially resistant against and survived kainic acid-induced seizures. JNK3 ko and JNK1 ko showed a nonsignificant tendency for decreased or increased death of hippocampal neurons, respectively. Surprisingly, the deletion of a single JNK isoform did not attenuate the immunocytochemical signal of phosphorylated c-Jun irrespective on the experimental set-up. This comprehensive study provides novel insights into the context-dependent physiological and pathological functions of JNK isoforms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2005.03857.x
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  • 6
    Electronic Resource
    Electronic Resource
    Antigen Presentation in MHC Class II Transgenic Mice: Stimulation versus Tolerization (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 117 (1990), S. 0 
    Details
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-065X.1990.tb00570.x
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  • 7
    Electronic Resource
    Electronic Resource
    Caspases and T lymphocytes: a flip of the coin? (2003)
    Oxford, UK : Munksgaard International Publishers
    Immunological reviews 193 (2003), S. 0 
    Details
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary:  In this review, we consider the role caspases play in cell death downstream of death receptors and cell intrinsic death mechanisms. In particular, we focus on these mechanisms in antigen-induced cell death, a mechanism which regulates the number of surviving T cells at the end of an immune response. The relative role of the apoptosome as an amplifier rather than an initiator of apoptosis is considered. Several factors that regulate the susceptibility to activation-induced cell death are considered. These factors emanate from the stimulation of the T-cell receptors and include multiple pathways. Recent work has shown that death receptor signaling can play an interesting role in cell proliferation in both humans and animals. These recent findings are discussed in the light of models of death receptor signaling.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1034/j.1600-065X.2003.00046.x
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  • 8
    Electronic Resource
    Electronic Resource
    Tumor necrosis factor-a and the progression of diabetes in non-obese diabetic mice (1999)
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 169 (1999), S. 0 
    Details
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: In the past decade, a wealth of information has accumulated through studies in non-obese diabetic (NOD) mice regarding the molecular and cellular events that participate in the progression to diabetes in insulin-dependent diabetes mellitus (IDDM). One molecule that has received considerable attention is the inflammatory cytokine tumor necrosis factor-a (TNF-α). TNF-a has been demonstrated to have a positive or negative effect on the progression to diabetes in NOD mice, although the mechanism by which TNF-α exerts these differential outcomes is unknown. Here we describe a new NOD model for analyzing the role of TNF-α in IDDM, TNF-α-NOD mice, TNF-cc-NOD mice express TNF-a solely in their islets from neonatal life onwards, and develop accelerated progression to diabetes. This rapid progression to diabetes is related to earlier and more aggressive infiltration of the islets with immune cells and an enhancement in the presentation of islet antigen in situ in the islets by islet-infiltrating antigen-presenting cells to T cells. Although adoptive transfer studies demonstrated that TNF-α can enhance presentation of islet antigen to both effector CD4- and CD8+ T cells, further investigations in TNF-α-NOD mice deficient in either CD4+ or CD8 *- T cells demonstrated that diabetes progression is dependent on CD8+ T cells, with CD4+ T cells playing a lesser role. The data accumulating from TNF-α-NOD mice, described in this review, indicates novel pathways by which inflammatory stimuli can precipitate autoimmunity, and suggests newer approaches in the design of therapeutic treatments that prevent β-cell destruction in IDDM.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-065X.1999.tb01302.x
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  • 9
    Electronic Resource
    Electronic Resource
    The Role of CD40 Ligand in Costimulation and T-Cell Activation (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Immunological reviews 153 (1996), S. 0 
    Details
    ISSN: 1600-065X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1600-065X.1996.tb00921.x
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  • 10
    Electronic Resource
    Electronic Resource
    Borrelia burgdorferi erpT expression in the arthropod vector and murine host (1999)
    Oxford BSL : Blackwell Science Ltd
    Molecular microbiology 31 (1999), S. 0 
    Details
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: The expression of a Borrelia burgdorferi gene, erpTwas investigated throughout the spirochaete life cycle in the arthropod vector and the murine host. Three phage clones from a B. burgdorferi DNA expression library synthesized a 30 kDa antigen that was recognized by antibodies in the sera of B. burgdorferi-infected mice but not mice hyperimmunized with B. burgdorferi lysates. Differential antibody binding suggested that this protein was preferentially expressed in vivo. This antigen was designated ErpT, based upon 99.6% homology with the BBF01 sequence in the B. burgdorferi genome. ErpT was not detected on spirochaetes cultured in BSK II medium by indirect immunofluorescence or in B. burgdorferi lysates by immunoblotting, implying that ErpT is not readily produced in vitro. erpT mRNA was not discernible by Northern blot but was identified by RNA polymerase chain reaction in vitro, indicating that erpT is expressed at low levels by cultured spirochaetes. erpT expression was then investigated in the vector and mice because B. burgdorferi do not normally reside in culture medium. RNA polymerase chain reaction and immunofluorescence studies demonstrated that erpT was expressed by a small minority of B. burgdorferi (11/500, 2.2%) within unfed ticks and then repressed during engorgement. erpT mRNA or ErpT antibodies were first detected in B. burgdorferi-infected mice at 4 weeks, suggesting that erpT was not expressed in the early stages of murine infection. Then, during persistent infection, RNA polymerase chain reaction showed that erpT was expressed by B. burgdorferi within the joints, heart and spleen, but not by spirochaetes in the skin. Immunization of mice with ErpT was antigenic but was not protective. These studies demonstrate that B. burgdorferi erpT is differentially expressed throughout the B. burgdorferi life cycle, in both the vector and the mammalian host, and is primarily expressed in extracutaneous sites during murine infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2958.1999.01171.x
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