AMLR AND LYMPHOID DIFFERENTIATION IN AIDS

获得性免疫缺陷综合征(AIDS)的特征是抑郁 与卡波西肉瘤和/或卡波西肉瘤相关的细胞免疫 机会性感染，通常见于同性恋男性，静脉注射药物 虐待者、血友病患者和哈田移民。抑郁的细胞介导的 免疫与胸腺肽Alpha1水平的升高是矛盾的， 提示缺乏T细胞谱系的前体和/或生物学上的 非活性胸腺肽α1。艾滋病被认为是一种 免疫失调表现为免疫细胞比例失衡 辅助性/抑制性T细胞表型。在自体混合淋巴细胞中 反应不同的T细胞亚群对非T细胞(T-Non T AMLR)或 活化的T细胞(T-T AMLR)和表达独特的免疫调节 功能。巨噬细胞产生的白细胞介素1促进 AMLR中IL-2的表达。因此，我们计划对AMLR进行研究，即考虑 免疫调节的基本模型，在艾滋病中。此外，我们会研究 胸腺上皮和胸腺因子对表型的诱导影响 和功能分化来描绘T细胞缺陷的水平(S) 在艾滋病方面。外周血淋巴细胞将进一步分离成T细胞 细胞、T细胞亚群(后经平移)和非T细胞。T细胞 在T-非T AMLR中激活将用作T-T AMLR中的刺激物。T细胞 在T-非T和T-T AMLR中激活将研究辅助/抑制 抗T细胞增殖和B细胞分化功能 空斑形成细胞实验中产生免疫球蛋白的细胞。这个 IL-2的产生(在IL-2依赖的T细胞系上测定)及其影响 将对AMLR上纯化的IL-2进行研究。粘附性巨噬细胞 用胸腺细胞有丝分裂试验检测内毒素和IL-1刺激的活性 化验。不同组份的骨髓和外周血单核细胞 将细胞与培养的胸腺上皮、胸腺培养 上清液，胸腺素V和胸腺素α1，并检查 应用单抗和流式细胞术表达分化抗原 有丝分裂原增殖反应分析仪，AMLR和免疫调节 功能。这些研究将有助于理解细胞和 免疫失调的分子基础及胸腺上皮的作用 及其产物在艾滋病的T细胞分化中的作用，这可能有助于 免疫缺陷管理中可能的免疫干预措施 在艾滋病方面。

Acquire immunodeficiency syndrome (AIDS) is characterized by depressed cell-mediated immunity associated with Kaposi's sarcoma and/or opportunistic infections, usually found in homosexual males, I.V. drug abusers, hemophiliacs and Hatian immigrants. The depressed cell-mediated immunity is in paradox with the elevated levels of thymosin Alpha1, suggests a lack of precursors of T cell lineage/or and biologically inactive thymosin Alpha1. AIDS is considered a syndrome of immunodysregulation characterized by imbalance of ratios of helper/suppressor T cells phenotypes. In the autologous mixed lymphocyte reaction distinct T cell subsets respond to non T cells (T-non T AMLR) or activated T cells (T-T AMLR) and express distinct immunoregulatory functions. Interleukin1 produced by macrophages enhances the production of IL-2 in the AMLR. Therefore, we plan to study the AMLR, that is considered a basic model of immunoregulation, in AIDS. Furthermore, we will study the inductive influence of thymic epithelium and thymic factors on phenotypic and functional differentiation to delineate the level of T cell defect(s) in AIDS. Peripheral blood lymphocytes will be further separated into T cells, T cells subsets (latter by panning) and non T cells. T cells activated in T-non T AMLR will be used as stimulators in T-T AMLR. T cells activated in T-non T and T-T AMLR will be studied for helper/suppressor functions against T cell proliferation and B cell differentiation to immunoglobulin producing cells in plaque forming cell assay. The production of IL-2 (measured on IL-2 dependent T cell line) and influence the purified IL-2 on the AMLR will be studied. Adherent macrophages are stimulated with LPS and IL-1 activity is measured by thymocyte mitogenic assay. Various fractions of bone marrow and peripheral blood mononuclear cells will be incubated with cultured thymic epithelium, thymic culture supernatants, thymosin V and thymosin Alpha1 and examined for the expression of differentiation antigens using monoclonal antibodies and FACS analyzer, proliferative response to mitogens, AMLR and for immunoregulatory functions. These studies will help in understanding the cellular and molecular basis of immunodysregulation and the role of thymic epithelium and its products in T cell differentiation in AIDS, that might help in possible immunological interventions in the management of immunodeficiency in AIDS.