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Neural immunoregulation: emerging roles for nerves in immune homeostasis and disease

IMMUNOLOGY TODAY 2000年第6期21卷 281-289页

作者： Downing, JEG Miyan, JA Univ London Imperial Coll Sci Technol & Med Sch Med Dept Neuroendocrinol London W6 8RF England Univ Manchester Inst Sci & Technol Dept Biomol Sci Manchester M60 1QD Lancs England

In this review, James Downing and Jaleel Miyan outline emerging evidence for neural mechanisms that contribute to specific categories of host defence. Involvement of direct innervation in the adaptive control of immunological responses complements an established view of neuroendocrine-immune modulation. The challenge remains to understand the integrative and homeostatic functions of 'hardwiring' of peripheral immune effector sites, its bearing on disorder and potential for therapeutic modification.

关键词：传入通路/生理学毛细血管通透性/生理学细胞运动肠神经系统/生理学糖皮质激素类/生理学内环境稳定下丘脑-垂体系统/生理学免疫系统/生理学肠黏膜/免疫学肠黏膜/神经支配杀伤细胞天然/免疫学肥大细胞/免疫学模型免疫学模型神经学神经纤维/生理学神经免疫调节/生理学神经元传入/生理学神经分泌系统/生理学垂体肾上腺系统/生理学脾/细胞学脾/免疫学应激/免疫学应激/病理生理学交感神经纤维节后/生理学交感神经系统/生理学迷走神经/生理学动物大鼠

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Intrathymic T cell development and selection proceeds normally in the absence of glucocorticoid receptor signaling

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IMMUNITY 2000年第2期13卷 179-186页

作者： Purton, JF Boyd, RL Cole, TJ Godfrey, DI Monash Univ Sch Med Dept Pathol & Immunol Prahran Vic 3181 Australia Baker Med Res Inst Prahran Vic 3181 Australia

Glucocorticoids are believed to play a role in T cell development and selection, although their precise function is controversial. Glucocorticoid receptor (GR)-deficient mice were used to directly investigate this problem. GR-deficient thymocytes were resistant to dexamethasone-mediated apoptosis, confirming the absence of glucocorticoid responsiveness. An absence of GR signaling had no impact on thymocyte development either in vivo or in vitro. T cell differentiation, including positive selection, was normal as assessed by normal development of CD4(+)CD8(+), alpha beta TCR(+)CD4(+), and alpha beta TCR(+)CD8(+) thymocytes. Negative selection, mediated by the superantigen staphylococcal enterotoxin B (SEB), or anti-CD3/CD28, was also normal in the absence of GR signaling. In contrast to earlier reports, these data demonstrate that GR signaling is not essential for intrathymic T cell development or selection.

关键词：细胞分化/生理学基因缺失基因表达调控发育期/生理学基因打靶糖皮质激素类/生理学器官培养技术受体糖皮质激素/生理学信号传导/生理学 T淋巴细胞/细胞学 T淋巴细胞/生理学胸腺/细胞学胸腺/胚胎学胸腺/生理学动物小鼠

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Delineation of the signaling pathways involved in glucocorticoid-induced and spontaneous apoptosis of rat thymocytes

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ENDOCRINOLOGY 2000年第2期141卷 528-538页

作者： Mann, CL Hughes, FM Cidlowski, JA NIEHS Lab Signal Transduct NIH Res Triangle Pk NC 27709 USA Univ N Carolina Curriculum Toxicol Chapel Hill NC 27599 USA

In primary rat thymocytes, both glucocorticoids and the withdrawal of in vivo survival factors elicit apoptosis. In this study we wanted to determine whether distinct pathways leading to apoptosis are engaged by these two stimuli. To address this question, we conducted a multiparametric analysis of cell viability, DNA fragmentation, activation of caspase-3-like activity, cell shrinkage, the loss of mitochondrial membrane potential, and externalization of phosphatidylserine in the absence and presence of protein and RNA synthesis. The role of caspase activity was also examined in both glucocorticoid- and survival factor withdrawal-induced cell death. We show that glucocorticoid-induced, but not spontaneous, loss of viability is dependent upon macromolecular synthesis and caspase activity. Furthermore, glucocorticoid-induced phosphatidylserine externalization and cell shrinkage are dependent upon gene regulation and caspase activity, whereas these features manifest independently of gene regulation and caspase activity in spontaneous death. In contrast, the loss of mitochondrial membrane potential was dependent upon macromolecular synthesis only in glucocorticoid-induced death and was independent of caspases in both spontaneous and dexamethasone-induced death. These results suggest that thymocytes can die by a caspase-independent mechanism and that a major difference between glucocorticoid- and survival factor deprivation-induced death is the dependence on gene expression.

关键词：肾上腺切除术膜联蛋白A5/分析细胞凋亡/药物作用细胞凋亡/生理学半胱氨酸天冬氨酸蛋白酶3 半胱氨酸天冬氨酸蛋白酶/代谢细胞大小细胞存活细胞培养的放线菌酮/药理学更生霉素/药理学地塞米松/药理学糖皮质激素类/药理学糖皮质激素类/生理学细胞内膜/药物作用细胞内膜/生理学动力学膜电位/药物作用膜电位/生理学线粒体/生理学磷脂酰丝氨酸类/代谢大鼠 Sprague-Dawley 信号传导/药物作用信号传导/生理学胸腺/细胞学胸腺/药物作用胸腺/生理学动物男(雄)性大鼠

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Five patients with biochemical and/or clinical generalized glucocorticoid resistance without alterations in the glucocorticoid receptor gene

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JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM 2000年第5期85卷 2076-2081页

作者： Huizenga, NATM De Lange, P Koper, JW De Herder, WW Abs, R Kasteren, JHLMV De Jong, F Lamberts, SWJ Univ Hosp Dijkzigt Dept Internal Med 3 NL-3015 GD Rotterdam Netherlands Univ Antwerp Hosp Dept Endocrinol B-2650 Antwerp Belgium St Anna Hosp Dept Pulm Dis NL-5664 EH Geldrop Netherlands

Cortisol resistance (CR) is a rare disease characterized by a generalized reduced sensitivity of end-organs to the actions of glucocorticoids (GCs). GC effects are mediated by the GC receptor (GR). The molecular alterations in CR described thus far were located in the hormone-binding domain of the GR gene. Recent reports of a considerable prevalence of abnormalities in the GR in patients attending the endocrine clinic prompted us to carry out further investigations with respect to GR protein and GR gene in patients attending the endocrine clinic for a broad spectrum of complaints and biochemical evidence suggesting a GR. In the present study, we describe five patients with biochemical and clinical CR. All patients showed a diurnal rhythm of serum cortisol concentrations (albeit at a high level), an insufficient suppression of serum cortisol concentration in reaction to 1 mg dexamethasone (DEX), and variable degrees of androgen overproduction, in the absence of clinical signs and symptoms of Cushing's syndrome. Three of the four female patients presented with complaints of androgen overproduction, two of them in combination with fatigue. The other female patient had severe steroid-resistant asthma. The only male patient and his son were asymptomatic. In four patients, we investigated receptor protein characteristics on mononuclear leukocytes in a whole cell DEX binding assay and studied the ability of DEX to inhibit mitogen-induced cell proliferation in mononuclear leukocytes in vitro. In all patients investigated, we found alterations in receptor number or ligand affinity and/or the ability of DEX to inhibit mitogen-induced cell proliferation. To investigate the molecular defects leading to the clinical and biochemical pictures in these patients, we screened the GR gene using PCR/single-strand conformational polymorphism/sequence analysis. No GR gene alterations were found in these patients. In conclusion, the five patients described had clinical and biochemical evi

关键词：雄激素类/生物合成地塞米松/药代动力学地塞米松/药理学抗药性糖皮质激素类/药理学糖皮质激素类/生理学多毛症氢化可的松/药理学氢化可的松/生理学淋巴细胞/药物作用淋巴细胞/生理学月经失调聚合酶链反应多态现象单链构象受体糖皮质激素/遗传学青少年成年人老年人女(雌)性人类男(雄)性

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Thymocyte resistance to glucocorticoids leads to antigen-specific unresponsiveness due to "holes" in the T cell repertoire

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IMMUNITY 2000年第2期12卷 183-192页

作者： Lu, FWM Yasutomo, K Goodman, GB McHeyzer-Williams, LJ McHeyzer-Williams, MG Germain, RN Ashwell, JD NCI Lab Immune Cell Biol NIH Bethesda MD 20892 USA NIAID Lymphocyte Biol Sect Immunol Lab NIH Bethesda MD 20892 USA Duke Univ Med Ctr Dept Immunol Durham NC 27710 USA

We have proposed that glucocorticoids antagonize TCR-mediated activation and influence which TCR avidities result in positive or negative selection. We now analyze the immune response of mice whose thymocytes express antisense transcripts to the glucocorticoid receptor (TKO mice). TKO mice responded normal ly to the complex antigen PPD but were proliferative nonresponders to pigeon cytochrome c 81-104 (PCC), having a large decrease in the frequency of PCC-responsive CD4(+) T cells. Unlike wild-type T cells, few TKO T cells in PCC-specific cell lines expressed V alpha 11(+)V beta 3(+). Furthermore, for naive CD4(+) T cells from unimmunized TKO mice, the frequencies of many of the molecular features common to the CDR3 regions of PCC-responsive V alpha 11(+)V beta 3(+) cells were substantially decreased. Thus, thymocyte glucocorticoid hyporesponsiveness resulted in loss of cells capable of responding to PCC, corresponding to an antigen-specific "hole" in the T cell repertoire.

关键词：细胞系细胞色素c组/免疫学细胞色素c组/药理学糖皮质激素类/生理学小鼠近交C57BL 小鼠转基因受体抗原 T细胞 α-β/免疫学受体糖皮质激素/生物合成受体糖皮质激素/遗传学受体糖皮质激素/免疫学 T淋巴细胞/药物作用 T淋巴细胞/免疫学胸腺/细胞学动物女(雌)性男(雄)性小鼠

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T-cell development and function - a downunder experience

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IMMUNOLOGY TODAY 2000年第10期21卷 472-474页

作者： Boyd, R Chidgey, A Monash Med Sch Dept Pathol & Immunol Prahran Vic Australia

It is nearly 40 years since Jacques Miller revealed the importance of the thymus as a major primary lymphoid organ. However, despite a vast number of subsequent publications confirming fhis, and defining many facets of thymopoiesis, it is clear that several key issues have remained unresolved. In order to review the enormous advances made in understanding the life of a T cell from precursor to pathology, the third 'ThymOz' meeting has been held in Australia*.

关键词：细胞分化减量调节基因重排糖皮质激素类/生理学配体主要组织相容性复合物/免疫学受体抗原 T细胞/遗传学受体抗原 T细胞/免疫学干细胞/免疫学间质细胞/免疫学 T淋巴细胞/免疫学 T淋巴细胞/生理学胸腺/细胞学胸腺/免疫学人类

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Delineation of an antiapoptotic action of glucocorticoids in hepatoma cells:: The role of nuclear factor-κB

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ENDOCRINOLOGY 2000年第5期141卷 1854-1862页

作者： Evans-Storms, RB Cidlowski, JA NIEHS Lab Signal Transduct NIH Res Triangle Pk NC 27709 USA

Glucocorticoids are primarily recognized for their profound antiinflammatory actions and their ability to induce lymphocyte apoptosis. We report here that, in contrast to their effect on cells of the immune system, glucocorticoids suppress serum deprivation induced apoptosis of rat hepatoma (HTC) cells. Suppression of apoptosis in these cells occurs at physiological concentrations of glucocorticoid and is abrogated by the glucocorticoid antagonist RU486. Although HTC cells also express receptors for progesterone, estrogen, and thyroid hormone, ligands for these receptors fail to rescue these cells from programmed cell death. Because the sensitivity of cells to apoptotic stimuli is often regulated by the ratio of antiapoptotic to proapoptotic Bcl-2 family members, we analyzed the influence of glucocorticoids and induction of apoptosis by serum starvation on the expression of these proteins. Bcl-2, Bcl-x(L), Bad, Bak, and Bar levels were not altered by either treatment. Mitochondrial function has recently been implicated as a critical early regulator of apoptosis in many cells including hepatocytes. Dexamethasone treatment blocked a decrease in this potential (Delta psi(m)) during serum deprivation induced apoptosis in HTC cells, indicating an action of this hormone upstream of mitochondria. We also show that the induction of apoptosis in HTC cells is associated with a decrease in nuclear factor (NF)-kappa B. Treatment with dexamethasone effectively blocked the loss of nuclear NF-kappa B, suggesting that this hormone acts to suppress apoptosis of HTC cells via regulation of this nuclear transcription factor. This hypothesis was confirmed by transfection experiments that show that expression of a superrepressor of NF-kappa B inhibits the ability of dexamethasone to rescue HTC cells from apoptosis induced by serum deprivation.

关键词：细胞凋亡细胞分裂细胞存活糖皮质激素类/生理学肝肿瘤实验性/病理生理学 NF-κB/生理学原癌基因蛋白质c-bcl-2/代谢肿瘤细胞培养的动物大鼠

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Differentiation of adipose stromal cells:: The roles of glucocorticoids and 11β-hydroxysteroid dehydrogenase

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ENDOCRINOLOGY 1999年第7期140卷 3188-3196页

作者： Bujalska, IJ Kumar, S Hewison, M Stewart, PM Univ Birmingham Queen Elizabeth Hosp Dept Med Birmingham B15 2TH W Midlands England

Glucocorticoids play an important role in determining adipose tissue distribution and function, with glucocorticoid excess states such as Cushing's syndrome resulting in central obesity. We have investigated the functional significance of local generation of cortisol within adipose tissue from inactive cortisone through the activity of the NADP(H)-dependent enzyme, 11 beta-hydroxysteroid dehydrogenase type 1(11 beta HSD1). In primary cultures of paired omental (om) and sc human adipose stromal cells (ASC;n = 34), 11 beta HSD1 oxo-reductase activity was significantly higher in om ASC (median, 40.2 pmol/mg protein.h;95% confidence interval, 1.8-105) compared with sc ASC (median, 11.4;95% confidence interval, 0-48.1;P < 0.001) despite similar endogenous NADPH/NADP concentrations. Both cortisol and insulin increased the differentiation of ASC to adipocytes (as assessed by glycerol-3-phosphate dehydrogenase expression), but only cortisol increased 11 beta HSD1 activity and messenger RNA levels in a dose-dependent fashion. Cortisone (500 nM) was as effective as 500 nM cortisol in inducing ASC differentiation, but this stimulatory effect was inhibited by coincubation with the 11 beta HSD1 inhibitor, glycyrrhetinic acid. The higher local conversion of cortisone to active cortisol through expression of 11 beta HSD1 in om compared with sc ASC may explain the specific action of glucocorticoids on different adipose tissue depots. 11 beta HSD1 expression in om ASC is regulated at a transcriptional level and is increased by glucocorticoids, but is not entirely dependent upon ASC differentiation. Inhibition of 11 beta HSD1 within om ASC inhibits cortisone-induced ASC differentiation. These findings indicate that local metabolism of glucocorticoid may control differentiation of adipose tissue in a site-specific fashion. Specific inhibitors of 11 beta HSD1 may offer a novel approach for the treatment of patients with central obesity.

关键词： 11-β-羟甾脱氢酶类脂细胞/细胞学脂肪组织/细胞学细胞分化/药物作用细胞分化/生理学细胞培养的可的松/药理学糖皮质激素类/生理学氢化可的松/药理学羟甾类脱氢酶类/遗传学羟甾类脱氢酶类/代谢羟甾类脱氢酶类/生理学胰岛素/药理学同工酶类/遗传学同工酶类/代谢同工酶类/生理学网膜 RNA 信使/代谢皮肤间质细胞/细胞学成年人老年人女(雌)性人类男(雄)性中年人

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Role of canonical glucocorticoid responsive elements in modulating expression of genes regulated by the arylhydrocarbon receptor

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DRUG METABOLISM REVIEWS 1999年第1期31卷 247-271页

作者： Linder, MW Falkner, KC Srinivasan, G Hines, RN Prough, RA Univ Louisville Sch Med Dept Biochem & Mol Biol Louisville KY 40292 USA Univ Texas Med Branch Dept Human Biol Chem & Genet Galveston TX 77550 USA Wayne State Univ Sch Med Dept Pharmacol Detroit MI 48201 USA

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关键词：细胞色素P450CYP1A1/遗传学基因表达调控基因报告糖皮质激素类/生理学肝/细胞学受体芳基烃/遗传学调控序列核酸动物人类大鼠

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Is the hypothalamic-pituitary-adrenal axis really hyperactivated in visceral obesity?

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JOURNAL OF ENDOCRINOLOGICAL INVESTIGATION 1999年第1期22卷 76-79页

作者： Kopelman, PG Univ London Queen Mary & Westfield Coll St Bartholomews & Royal London Sch Med & Dent London E1 4NS England

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