Advances in Neuroimmunology

William P. Halford

Daniel J.J. Carr

Adv Neuroimmunol

Subversion of intracellular signal transduction by Herpes simplex virus type 1

单纯疱疹病毒1型对细胞内信号转导的颠覆

Mark R. Opp

Foreword

前言

The role of classical neurotransmitters in sleep regulation is amply documented (Hobson and Steriade, 1986). In recent years evidence has been gathered that immunoactive molecules, infectious agents and their components, or cytokines play some part in sleep regulation (Krueger and Obál, 1994; Opp et al., 1992; Moldofsky, 1994). Different cytokines possess hypnogenic properties when injected centrally or systemically to different animal species and their role in physiological sleep regulation is currently under investigation. Little is known of how cytokines and classical neurotransmitters interact and of the relevance of this interaction in sleep induction and maintenance. The present paper (i) reviews data on this topic; (ii) proposes a unitary interpretation whenever possible; and (iii) raises questions that might be addressed by future studies.

Maria Grazia De Simoni

Luca Imeri

Walter De Matteo

Carlo Perego

Sylvie Simard

Salvatore Terrazzino

Sleep regulation: Interactions among cytokines and classical neurotransmitters

睡眠调节：细胞因子和经典神经递质之间的相互作用

Starting in the 1950s through the 1980s, clinical practice has evolved to essentially eliminate classic kernicterus. Great strides have been made in the management of neonatal jaundice, hyperbilirubinemia, and prevention of kernicterus over the past 25 years. The American Academy of Pediatrics practice parameter on the management of jaundice, published in 2004 and updated in 2009, marked a shift in clinical practice that initially resulted in a large decrease in the number of children developing kernicterus. However, a reemergence of kernicterus occurred in recent years and continues to the present. This has been associated with changes in medical practice and health care delivery. Importantly, universal screening of infants combined with close follow-up, monitoring, and aggressive phototherapy treatment at relatively low bilirubin levels could eliminate most of the new cases of kernicterus, but the prevention of a devastating but very rare disorder must be balanced against the costs and possible risks of overtreating a very large numbers of infants. Determining the bilirubin level at which toxicity is increased is a difficult issue for physicians in everyday practice. This must be balanced against the gains of an early visit versus the concerns that increased surveillance will result in a greater use of resources (phototherapy), more parental anxiety, and reduced breastfeeding. Gaps in knowledge persist, including the neurotoxic impact of hyperbilirubinemia in preterm infants, and the potential importance of genomic susceptibility to bilirubin neurotoxicity.

S B Churn

Multifunctional calcium and calmodulin-dependent kinase II in neuronal function and disease

神经元功能与疾病中的多功能钙调蛋白依赖性蛋白激酶II

Many of the known roles of arginine (e.g. in immune function, wound healing, and protection against ammonia intoxication) are mediated by a metabolic pathway synthesising nitric oxide (NO) in the liver. Contrary to some of the current views, liver-produced NO may be basically beneficial, as it exerts both protective actions against tissue injury and cytotoxic effects on invading microorganisms, parasites, or tumor cells. An ongoing equilibrium between NO and other NO-reactive compounds (e.g. O2 and non-heme iron-sulphur-containing moieties) appears to be important in this respect, even under critical conditions. Thus, NO may prevent liver tissue harm from oxidant stress. Only when this putative counterbalance is upset by an uncontrolled, prolonged and/or massive production of NO, liver tissue damage may occur leading to hepatic inflammation or even tumor development. Moreover, the currently available data support the working hypothesis that hepatocytes partake not only to immunoregulatory processes, but even to immune defence mechanisms. Thus, the liver constitutes an excellent model for investigations into the crosstalks regulating the production of NO which take place among not only the various networks operating inside a single hepatic cell, but even the individual types of liver cells.

Hisanori Suzuki

Marta Menegazzi

Alessandra Carcereri de Prati

Sofia Mariotto

Ubaldo Armato

Nitric oxide in the liver: Physiopathological roles

一氧化氮在肝脏中的生理病理作用

RosaP. Gomariz

Preface

George B. Stefano

Eric M. Smith

Editorial announcement

编者按

Evidence for VIP influences on immune function comes from studies demonstrating VIP-ir nerves in lymphoid organs in intimate anatomical association with elements of the immune system, the presence of high-affinity receptors for VIP, and functional studies where VIP influences a variety of immune responses. Anatomical studies that examine the relationship between VIP-containing nerves and subpopulations of immune effector cells provide evidence for potential target cells. Additionally, the presence of VIP in cells of the immune system that also possess VIP receptors implies an autocrine function for VIP. The functional significance of VIP effects on the immune system lies in its ability to help coordinate a complex array of cellular and subcellular events, including events that occur in lymphoid compartments, and in musculature and intramural blood circulation. Clearly, from the work described in this chapter, the modulatory role of VIP in immune regulation is not well understood. The pathways through which VIP can exert an immunoregulatory role are complex and highly sensitive to physiological conditions, emphasizing the importance of in vivo studies. Intracellular events following activation of VIP receptors also are not well elucidated. There is additional evidence to suggest that some of the effects of VIP on cells of the immune system are not mediated through binding of VIP to its receptor. Despite our lack of knowledge regarding VIP immune regulation, the evidence is overwhelming that VIP can interact directly with lymphocytes and accessory cells, resulting in most cases, but not always in cAMP generation within these cells, and a subsequent cascade of intracellular events that alter effector cell function. VIP appears to modulate maturation of specific populations of effector cells, T cell recognition, antibody production, and homing capabilities. These effects of VIP are tissue-specific and are probably dependent on the resident cell populations within the lymphoid tissue and the surrounding microenvironment. Different microenvironments within the same lymphoid tissue may influence the modulatory role of VIP also. Effects of VIP on immune function may result from indirect effects on secretory cells, endothelial cells, and smooth muscle cells in blood vessels, ducts, and respiratory airways. Influences of VIP on immune function also may vary depending on the presence of other signal molecules, such that VIP alone will have no effect on a target cell by itself, but may greatly potentiate or inhibit the effects of other hormones, transmitters, or cytokines. The activational state of target cells may influence VIP receptor expression in these cells, and therefore, may determine whether VIP can influence target cell activity. Several reports described in this chapter also indicate that VIP contained in neural compartments is involved in the pathophysiology of several disease states in the gut and lung. Release of inflammatory mediators by cells of the immune system may destroy VIP-containing nerves in inflammatory bowel disease and in asthma. Loss of VIPergic nerves in these disease states appears to further exacerbate the inflammatory response. These studies indicate that altered VIP concentration can have significant consequences in terms of health and disease. In addition, the protective effects of VIP from tissue damage associated with inflammatory processes described in the lung also may be applicable to other pathological conditions such as rheumatoid arthritis, anaphylaxis, and the swelling and edema seen in the brain following head trauma. While VIP degrades rapidly, synthetic VIP-like drugs may be developed that interact with VIP receptors and have similar protective effects. Synthetic VIP-like agents also may be useful in treating neuroendocrine disorders associated with dysregulation of the hypothalamic—pituitary—adrenal axis, and pituitary release of prolactin.

Denise L. Bellinger

Dianne Lorton

Sabine Brouxhon

Suzanne Felten

David L. Felten

The significance of vasoactive intestinal polypeptide (VIP) in immunomodulation

血管活性肠肽（VIP）在免疫调节中的重要性

Small intestine intraepithelial lymphocytes (IELs) comprise a heterogeneous and phenotypically complex population of T cells that are part of the gut-associated lymphoid tissues (GALTs). Recent studies from a number of laboratories indicate that murine IELs are greatly enriched for extrathymic T cells, although many aspects of the IEL+ extrathymic developmental pathway remain controversial, and there is currently no consensus of opinion as to which IELs are extrathymic and which are thymus-derived. Those differences reflect variations in the IEL repertoire in athymic animals depending upon the specific model used to study IELs, and they correlate with the age at which mice became or were rendered athymic, implying that the thymus participates either directly or indirectly in the local extrathymic IEL developmental process. In this article, the basic findings regarding intestinal T cell development are discussed, and a hypothesis is provided which links neuroendocrine interactions targeted to the intestine epithelium to the striking relationship between animal developmental age and the thymopoietic potential of the intestine.

John R. Klein

T cell development within the intestinal mucosa: Clues to a novel immune-endocrine network?

肠黏膜中的T细胞发育：揭示新型免疫-内分泌网络的线索？

Our previous studies have shown that prolactin (PRL), a pituitary and lymphocyte hormone and a ligand of the cytokine/hemopoietin receptors (R) superfamily, acts synergistically with interleukin (IL)-2 on the development of lymphokine activated killer (LAK) cells and enhances the effects of GM-CSF and IL-3 on myeloid progenitors' proliferation and differentiation. More recently, we have demonstrated that GM-CSF and IL-3 increase the sensitivity of acute myeloid leukemic (AML) cells to LAK activity. Together, these findings have prompted us to study the role of PRL on the target arm of the LAK response. We show here that CD33+ blasts from AML patients express membrane PRL-R and that the PRL/PRL-R interaction is followed by increased susceptibility to natural killer (NK) (p < 0.02) and LAK (p < 0.001) cells. As predicted from the dimerization model of PRL-R and in agreement with previous reports, the response of AML blasts to PRL was bell-shaped with a trend peak at 25 ng/ml. Although enhanced lysis occurred at the target recognition level, it was not accompanied by changes in the MHC class I, cellular adhesion molecules, or myeloid differentiation antigens. Cell cycle recruitment and lysis increased concurrently in three cases studied, suggesting a modulatory action of PRL on the expression of putative cycle-related NK/LAK-target structures. Together, these data strengthen the role of PRL in the LAK response.

E. Oberholtzer

M. Contarini

F. Veglia

A. Cossarizza

C. Franceschi

M. Geuna

M. Provinciali

G. Di Stefano

J. Sissom

M.F. Brizzi

L. Pegoraro

L. Matera

Prolactin increases the susceptibility of primary leukemia cells to NK and LAK effectors

催乳素增加原发性白血病细胞对NK和LAK效应细胞的敏感性

出版信息	出版商: Elsevier B.V.，出版周期: ，期刊类型: journal，开源期刊: 否
基本数据	创刊年份: 1991，原创研究文献占比: ，自引率:， Gold OA占比:

Advances in Neuroimmunology

期刊引文格式

有 1 位以上作者的期刊

有 2 位作者的期刊

有 3 位作者的期刊

有 5 位以上作者的期刊

书籍引用格式

学位论文引用格式

网页引用格式

专利引用格式

手工熬夜修改参考文献？研飞自动匹配期刊，一键轻松成稿，支持 Word/WPS

投稿经验分享