STRESS & IMMUNITY; BEHAVIORAL & PHYSIOLOGICAL MECHANISMS

最近，人们对两国之间的潜在关系很感兴趣 暴露于应激源和免疫系统的功能。这是 因为免疫功能的改变可能会调节 从艾滋病到癌症，各种疾病的发展都有压力。 事实上，一直有人认为，关于个人差异的 人类免疫缺陷病毒感染后艾滋病症状的发展和表现 部分归因于心理或生理上的 在对病毒的免疫反应中处于关键阶段的压力。 这项建议关注的是体内免疫功能的变化。具体的 建议的目的是：1)研究行为因素，这些因素包括 在确定应激源暴露是否以及如何改变 抗猪传染性支气管炎病毒特异性抗体和抗体分泌细胞的形成 抗原(Ag)K1H。尽管已经有许多示威活动， 暴露在痛苦或令人厌恶的事件中会改变免疫力的某些方面 函数，但针对隔离的分析工作很少。 重要的行为调节因素。在这里，我们希望集中讨论2 因素：a)应激源的行为可控性，两者都是在休克中 和击败范式，b)统治。2)研究神经和神经内分泌 研究应激条件的介质会改变抗体水平。焦点 是在两个不同但相关的问题上。A)中枢神经系统 在压力源和外周变化之间起调节作用的过程 可以接触到免疫器官和细胞。去甲肾上腺素能(NE)过程 与下丘脑室旁核(PVN)相关 受到特别的关注。PVN是一种关键的控制结构 垂体-肾上腺和交感-肾上腺延髓的活动，以及NE 对PVN的输入是一个主要的刺激因素。B)外围设备 应激产生抗体的神经内分泌介质 改变。这里的重点将是阐明肾上腺的作用 肾上腺髓质释放的皮质类固醇和血浆儿茶酚胺 和感同身受的终端。 3)研究应激源及其神经和免疫功能的变化。 神经内分泌后遗症可能是抗体降低的原因 形成，重点将放在应激源产生的细胞变化上 在免疫间隔之间的贩运，导致改变的比率 淋巴细胞表型。

There is considerable recent interest in potential relationships between exposure to stressors and the functioning of the immune system. This is because alterations in immune function might mediate the impact of stressors on the development of diseases ranging from AIDS to cancer. Indeed, it has been argued that individual differences concerning the development and expression of AIDS symptoms from infection with HIV might be partially accounted for by the occurrence of psychological or physical stress at a critical stage in the cascade of immune reactions to the virus. This proposal focuses on in vivo changes in immune function. The specific aims of the proposal are: 1) To study behavioral factors which are important in determining whether and how stressor exposure will alter the formation of specific antibody (Ab) and Ab secreting cells (ASCs) to the antigen (Ag) KLH. Although there have been numerous demonstrations that exposure to painful or aversive events can alter some aspect of immune function, there has been very little analytic work directed at isolating important behavioral modulating factors. Here we wish to focus on 2 factors: a) Behavioral controllability of the stressor, both in the shock and defeat paradigms, b) Dominance. 2) To study neural and neuroendocrine mediators by which the stress conditions studied alter Ab levels. Focus is on 2 different but related issues. a) The central nervous system processes that mediate between the stressor and the peripheral changes that could contact immune organs and cells. Noradrenergic (NE) processes associated with the paraventricular nucleus (PVN) of the hypothalamus will receive particular attention. The PVN is a key structure in controlling both pituitary-adrenal and sympathoadrenomedullary activity, and the NE input to the PVN is a major stimulatory factor. b) The peripheral neuroendocrine mediators that are responsible for the stress-produced Ab changes. Here emphasis will be on elucidating the roles of adrenal corticosteroids and plasma catecholamines released by the adrenal medulla and sympathetic terminals. 3) To study immunologic changes produced by stressors and their neural and neuroendocrin sequelae that might be responsible for the reduced Ab formation, the focus will be on stressor produced alterations in cell trafficking between immune compartments, resulting in changed ratios of lymphocyte phenotypes.