EPIDEMIOLOGY OF HD IN TWINS--INFECTIONS/T-CELL FUNCTION

几条流行病学证据表明，年轻人 霍奇金氏病是由较晚接触一种或多种 感染性病原体，可能包括爱泼斯坦-巴尔病毒等 表示此情况以意外的高频率在 其他HD病例的血缘关系。临床和实验室研究 指出T辅助细胞功能异常为主要缺陷 在这种疾病中。越来越明显的是，在老鼠和人类中，T-helper都是 细胞(Th细胞)或多或少地克隆成两种类型， 表示为Th1和Th2，可以根据 不同外源物质诱导的细胞因子分泌模式 可能是相互抑制的，似乎起作用的药物 不同的功能。Th1细胞促进细胞介导的免疫反应， Th2细胞促进体液免疫的激活。EBV基因组 包含一个可以模拟某些Th2函数的组件。我们 假设HI)发生在受抑制的细胞介导的条件下 由Th2基因决定的优势诱导的免疫活性 功能，随后抑制Th1功能，有或没有 EBV感染对Th1的协同抑制作用 不接触其他感染源，遵循脊髓灰质炎模型 年龄特定的疾病易感性。我们建议研究的子集 双胞胎不一致的HI)通过I)比较Th分泌谱 病例及其健康同卵双胞胎与无血缘关系的同卵双胞胎 2)比较患者与健康人的抗EBV抗体效价 与健康的无血缘关系的人的同卵双胞胎，3) 病例和受试者V-βT细胞受体谱系的比较 健康的同卵双胞胎病例与无血缘关系的人的病例。

Several lines of epidemiologic evidence suggest that young adult Hodgkin's disease is determined by late exposure to one or more infectious agents, possibly including Epstein-Barr virus, and other lines indicate that this conditions occurs with unexpectedly high frequency in the blood relatives of other HD cases. Clinical and laboratory studies point to a T-helper cell functional abnormality as the primary deficit in this disease. It is becoming clear that in both mouse and man T-helper cells (Th cells) clone more or less -dichotomously into two types, designated Th1 and Th2, which can be differentiated on the basis of the cytokine secretion pattern, which are induced by different exogenous agents, which may be mutually inhibitory, and which appear to serve different functions. Th1 cells promote the cell-mediated immune response, and Th2 cells promote activation of humoral immunity. The EBV genome contains a component that may simulate certain Th2 functions. We hypothesize that HI) occurs in a condition of suppressed cell-mediated immunocompetence, induced by a genetically determined predominance of Th2 function, with consequent suppression of Th1 function, with or without synergistic suppression of Th1 as a result of EBV infection, and with or without exposure to other infectious agents, following the polio model of age-specific disease susceptibility. We propose to study subsets of twin pairs discordant for HI) by I) comparing the Th secretion profiles of cases and their healthy identical co-twins to that of unrelated persons, 2) comparing the anti-EBV antibody titers of cases their healthy identical co-twins with those of healthy unrelated persons, and 3) comparing the V-Beta T-cell receptor repertoire of cases and their healthy identical co-twins of cases to those of unrelated persons.