| 书目名称 | Steroid Hormones and the T-Cell Cytokine Profile | | 编辑 | G. A. W. Rook,S. Lightman | | 视频video | http://file.papertrans.cn/878/877454/877454.mp4 | | 图书封面 |  | | 出版日期 | Book 1997 | | 关键词 | asthma; autoimmune disease; bacteria; cytokine; diseases; glucocorticoid; hormone; hypothalamus; metabolism; | | 版次 | 1 | | doi | https://doi.org/10.1007/978-1-4471-0931-0 | | isbn_softcover | 978-1-4471-1238-9 | | isbn_ebook | 978-1-4471-0931-0 | | copyright | Springer-Verlag London Limited 1997 |
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Front Matter |
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Abstract
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,Mechanisms of action of cytokines on the central nervous system. Interaction with glucocorticoids, |
Robert Dantzer,Sophie Layé,Emmanuelle Goujan,Rose-Marie Bluthé,Jan Pieter Konsman,Patricia Parnet,Ke |
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Abstract
Interleukin-1 (IL-1), IL-6 and tumour necrosis factor-alpha (TNF.) are multifunctional cytokines which are released by activated monocytes and macrophages and play a pivotal role in inflammation and infection [1]. Although their biological activities widely overlap, each cytokine has its own characteristic properties. IL-1 exists in two molecular forms, IL-1. and IL-l., which are encoded by different genes. Another member of the IL-1 family is the interleukin-1 receptor antagonist (IL-lra). This cytokine behaves as a pure endogenous antagonist of IL-1 receptors and blocks most biological effects of IL-l. and IL-l. in vivo and in vitro. IL-6 is mainly responsible for the synthesis of acute phase proteins by hepatocytes. TNF. plays a major role in the pathogenesis of the acute shock syndrome. Although all of these cytokines are produced mainly by activated monocytes and macrophages, they are also synthesized by a wide variety of immune and non-immune cells, including glia and neurons [2]. IL-1, IL-6 and TNF. have potent effects in the central nervous system, resulting in fever, induction of sickness behaviour, and activation of the hypothalamic-pituitary-adrenal (HPA) axis [3].
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,Signals from the hypothalamus to the pituitary during chronic immune responses, |
Michael S. Harbuz,Stafford L. Lightman |
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Abstract
The question of whether stress is good or bad is a pertinent one in relation to pathology. A major component of the host response to stress is the activation of the hypothalamo-pituitary-adrenal (HPA) axis. The end point of this activation is the release of glucocorticoid steroid hormones from the adrenal cortex (predominantly corticosterone in the rat and cortisol in man). The importance of this system to the integrity of the individual can be demonstrated by investigating the extreme situation where the adrenal is removed or no longer functioning. This situation can be created surgically in experimental animals and occasionally in humans, although more frequently it occurs as a result of defective function of the adrenals due to autoimmune disease or tuberculosis leading to adrenal insufficiency (Addison’s disease). In patients with Addison’s disease minor challenges which might only produce mild symptoms in a normal individual can be life threatening. An interesting parallel to this can be seen following injection of the cytokine interleukin-1 (IL-1) or the immune stimulant lipopolysaccharide (LPS) an agent which produces flu-like symptoms for a few hours when given to humans. D
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,The role of the innervation of lymphoid tissue in the regulation of the Th1/Th2 dichotomy, |
Barbara Kruszewska,Jan A. Moynihan,David L. Felten |
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Abstract
Immune responses can be modulated by input from the sympathetic nervous system (SNS) [reviewed in 1–3]. There is ample evidence that the components necessary for such an interaction are present in a normal animal. Histological studies clearly show the presence of nerve fibres within synaptic distance of cells in many lymphoid tissues, including spleen, lymph nodes, thymus and bone marrow [4,5]. These postganglionic sympathetic nerve fibres release norepinephrine (NE) as the major neurotransmitter, and are visualized easily with immunocytochemical methods utilizing antibodies to tyrosine hydroxylase, the rate-limiting enzyme in NE synthesis. Nerve fibres staining for numerous neuropeptides also have been found in these lymphoid organs; a role for these other neurotransmitters (such as neuropeptide Y) has not been elucidated fully. Norepinephrine is the most prominent neurotransmitter candidate in sympathetic postganglionic nerve fibres and therefore has been the focus of extensive research.
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,Modulation of glucocorticoid activity by metabolism of steroids in non-lymphoid organs, |
Brian R. Walker |
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Abstract
The adrenal cortex secretes three classes of steroid hormones: mineralocorticoids, androgens and glucocorticoids [1]. In rodents the principal glucocorticoid is corticosterone, but in humans cortisol (i.e. 17.-OH-corticosterone) is more abundant because 17-hydroxylase is expressed in adrenal fasciculata/reticularis cells. This enzyme also accounts for greater production of adrenal androgens (dehydroepiandrosterone and androstenedione) in humans than in rodents. A wide variety of synthetic glucocorticoids is available, in most of which affinity for the glucocorticoid receptor is increased by inclusion of a halogen group in the 9.-position, as in beclomethasone or dexamethasone.
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,Microenvironmental control of glucocorticoid functions in immune regulation, |
Jon D. Hennebold,Raymond A. Daynes |
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Abstract
Lipophilic hormones, including the steroids, thyroid hormones, retinoids, 1,25 dihydroxyvitamin D., members of the prostaglandin J. series, and leukotriene B. represent a diverse group of molecules that can regulate gene expression through a common molecular mechanism. This diverse set of ligands traverse the plasma membrane and bind to ligand-specific intracellular receptors present within the cytosol, perinuclear space, or the nucleus of responsive cell types. Once activated by ligand binding, these intracellular receptors, which are all members of the steroid/nuclear receptor superfamily bind to specific sites on DNA and function as enhancers or repressors of gene transcription [1,2].
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,Immunological consequences of inhibiting dehydroepiandrosterone (DHEA) sulfatase in vivo, |
Roly Foulkes,Stevan Shaw,Amanda Suitters |
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Abstract
The host response to combat invasion of infectious agents needs to be rapid, flexible, effective and above all coordinated. Recognition and elimination of antigen is usually a very efficient process, requiring the integrated activity of a variety of cell types. It is the recruitment and activation of these cells that leads to an appropriate immune response. Indeed an inappropriate immune response can often lead to pathology such as that seen in autoimmune disease and allergy.
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,Corticosterone and the hypothalamic-pituitary-adrenal (HPA) axis in autoimmune diseases, |
Francisco Ramírez,Don Mason |
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Abstract
Antigen-specific immune responses, which have evolved to protect the mammalian host from disease-causing organisms, are elicited when lymphocytes recognize pathogen-derived antigens and receive simultaneously the appropriate co-stimuli from the antigen-presenting cell. Following the initial triggering steps the immune system can activate a variety of effector mechanisms to eliminate or control the pathogenic organisms that produce the antigens in question. The activation and the development of effector mechanisms are complex events which require the participation of many components of the immune system. As many of the biological parameters are susceptible to genetic variation, it is not surprising that inbred strains of laboratory animals differ strikingly in the way that they respond to various antigens. The differences concern two aspects of immunity.
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,Glucocorticoid regulation of , in host resistance to mycobacteria, |
David H. Brown,Bruce S. Zwilling |
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Abstract
The ability of glucocorticoid hormones to effectively modulate an immune response has been widely studied. Glucocorticoid production and release from the adrenal cortex is stimulated primarily by adrenocorticotrophin (ACTH), which in turn, is controlled by Corticotrophin-releasing hormone (CRH) derived from the hypothalamus [1]. Circadian rhythms or “episodic” increases and decreases occur during each day. Stress overrides feedback regulation of glucocorticoid levels resulting in elevated levels of glucocorticoids. Alterations in corticosterone levels results in either an enhancement or suppression of defence mechanisms. Glucocorticoids, which freely penetrate the cell, bind to their cytoplasmic receptor [2]. The hormone-receptor complex translocates to the nucleus and binds to regulatory elements associated with certain genes (glucocorticoid response elements), which can activate or inhibit transcription of those genes. Glucocorticoids probably have primary and secondary cell targets. Primary targets are affected directly by glucocorticoids through the binding of the hormone to its receptor, whereas secondary target cells are affected by mediators (cytokines) produced by primary t
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,Human and murine tuberculosis as models for immuno-endocrine interactions, |
G. A. W. Rook,R. Hernandez-Pando,R. Baker,H. Orozco,K. Arriaga,L. Pavon,M. Streber |
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Abstract
Recent studies of human and murine tuberculosis have revealed striking changes in adrenal steroid output and metabolism. In this review we use tuberculosis as a model on which to base discussion of the ways in which these changes, even when not disease-specific, may impact upon the function of T lymphocytes during chronic inflammation. Other chapters in this volume amplify further several of the topics highlighted in this one.
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Back Matter |
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Abstract
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