INTERACTIONS OF CELLULAR AND HUMORAL IMMUNITY

关于干扰素(IFN)在MODU中的可能作用的研究正在计划中。 系统性红斑狼疮和结缔组织病等结缔组织疾病的免疫反应 拉。细胞起源，生产的控制机制以及 对体液免疫和细胞免疫体外模型的影响 特别注意酸不稳定的α-干扰素(AL-α-干扰素) 已知其在系统性红斑狼疮血清中升高。将分离出阿尔法干扰素 用琼脂糖连接抗-α-干扰素-抗-干扰素的亲和层析柱 尸体。AL-α干扰素与非酸不稳定α-干扰素的比较 它们对自然杀伤细胞功能的影响以及在体外的研究 B细胞功能和T细胞活化。可能的直接参与 α-干扰素在狼疮肾小球肾炎免疫复合体病变中的作用 与各种其他慢性肾脏疾病同时进行的研究。 α-干扰素在肾脏和皮肤组织中的沉积将通过 间接免疫荧光及其与α-干扰素的可能相互作用 测量免疫复合体或肾小球基底膜的成分。 类风湿性关节炎患者的滑膜组织将被研究 α和γ-干扰素的产生及对γ-干扰素释放的调节作用 用短期滑膜组织细胞培养法检测前列腺素E_2。 从共培养的滑膜组织中释放物质的可能性 可能通过外周血单个核细胞诱导产生干扰素 学习。此外，抗淋巴因子等内源性因素的作用 细胞抗体、假定的自身抗原(DNA、自体聚集的免疫球蛋白、 核苷酸或核酸)将刺激干扰素的释放 检查过了。还将尝试确定这两种阿尔法干扰素 和伽玛干扰素与任何容易证明的 免疫控制机制。最后，将对伽玛干扰素进行研究。 对体外T和B细胞相互作用的影响。

Studies are planned on the possible role of interferons (IFNS) in modu- lating the immune response in connective tissue diseases such as SLE and RA. Cellular origin, controlling mechanisms of production as well as influence on in vitro models of humoral and cell-meidated immunity will be examined with particular attention to acid-labile Alpha IFN (AL Alpha IFN) which is known to be elevated in SLE serum. AL Alpha IFN will be isolated by affinity columns composed of sepharose linked to anti-Alpha IFN anti- body. Comparison of AL Alpha IFN and non acid labile Alpha IFN will be made for their effects on Natural Killer cell function as well as in vitro B cell function and T cell activation. Possible direct participation of Alpha IFN in immune complex lesions of lupus glomerulonephritis will be studies in parallel with a wide variety of other chronic renal diseases. Renal and skin tissue deposition of Alpha IFN will be determined by indirect immunofluorescence and possible interactions between Alpha IFN and components of immune complexes or glomerular basement membrane measured. Synovial tissues from patients with rheumatoid arthritis will be studied for both a and Gamma IFN production and modulation of Gamma IFN release by prostaglandin E2 examined, using short-term synovial tissue cell cultures. The possibility that materials released from co-cultured synovial tissues may induce IFN production by peripheral blood mononuclear cells will be studied. In addition the role of endogenous factors such as anti-lympho- cyte antibodies, putative autoantigens (DNA, autologous aggregated IgG, nucleotides, or cucleic acids) in stimulating IFN release will be examined. An attempt will also be made to determine whether both Alpha IFN and Gamma IFN are produced in conjunction with any easily demonstrable immune control mechanisms. Finally Gamma IFN wil be studied for its demonstrable effect on in vitro T and B cell interaction.