NEURAL ASPECTS OF IMMUNE DEFICIENCY

拟议的项目将确定脑内神经免疫的相互作用 自发性高血压大鼠(SHR)存在免疫缺陷 以及增加的交感神经活动。压力和交感神经活动 可能是免疫系统的重要调节剂，并可能导致 免疫能力下降。免疫无能或免疫缺陷是一种 在艾滋病患者和那些人身上看到的重要医学问题 由于器官移植导致的免疫抑制。在艾滋病患者中，压力是 这是缩短艾滋病毒潜伏期的一个促成因素。 通过更好地了解免疫系统的神经调节， 有可能提高普通人群的健康，并 还通过增加潜伏期和减少 症状的严重程度。SHR可能会被证明是一个有价值的模型 目的：一旦其免疫缺陷和交感神经支配的免疫 器官的特性更好了。拟议项目的目标是：1) 自发性高血压大鼠与Wistar大鼠免疫缺陷的比较 京都(WKY)大鼠通过检测；淋巴细胞亚群，产生 特定抗体，对外来细胞的反应能力，生物活性 T淋巴细胞生长因子白介素2与脾、胸腺的检测 大小/组织学。2)研究交感神经支配的特点 SHR和WKY大鼠胸腺和脾的组织化学研究 免疫组织化学和放射酶分析方法。3)确定是否 交感神经支配与神经传导之间存在因果关系 自发性高血压大鼠的免疫缺陷 免疫系统切除对自发性高血压大鼠免疫功能的影响。在这次评估中， 将检查免疫功能、脾/胸腺大小和组织学。 自发性高血压模型可能被证明对以下两方面都有价值：a)从神经学角度理解 诱发免疫缺陷和b)测试提高免疫力的药物疗效 免疫缺陷者(即艾滋病患者)的功能。

The proposed project will determine the neuroimmune interaction in the spontaneously hypertensive rat (SHR) which possesses an immune deficiency and an increased sympathetic activity. Stress and sympathetic activity are potentially important modulators of the immune system and can lead to decreased immunologic competence. Immune incompetence or deficiency is an important medical problem seen in both AIDS patients and those immunosuppressed because of organ transplants. In AIDS patients, stress is a contributing factor in reducing the latency period of the HIV virus. Through a better understanding of neural regulation of the immune system, it may be possible to increase the health of the general population and also help AIDS patients by increasing the latency period and decrease the severity of the symptoms. The SHR may prove a valuable model for these purposes, once its immune deficit and sympathetic innervation of immune organs are better characterized. The aims of the proposed project are: 1) to characterize the immune deficiency of the SHR compared to the Wistar Kyoto (WKY) rat by examining; lymphocyte subsets, ability to generate specific antibodies, ability to react to foreign cells, bioactivity of the T-lymphocyte growth factor Interleukin-2 and examine spleen and thymic sizes / histology. 2) To characterize the sympathetic innervation of thymus and spleen in SHR and WKY rats using histochemical, immunohistochemical and radioenzymatic assay methods. 3) To determine if there is a causal relationship between the sympathetic innervation and immune deficiency in the SHR, by examining the effect of immunosympathectomy on the SHR immune function. For this evaluation, immune function and splenic/thymic sizes and histology will be examined. The SHR model may prove to be valuable for both: a) understanding neurally induced immunodeficiency and b) testing drug efficacy for increasing immune function in the immune deficient subject (i.e. AIDS patients).