INTERACTIONS OF CELLULAR AND HUMORAL IMMUNITY

计划研究干扰素（IFNS）在调制中的可能作用， 在结缔组织疾病如SLE和 RA. 细胞起源，控制生产机制以及 对体液免疫和细胞介导免疫体外模型的影响， 特别注意酸不稳定α IFN（AL α IFN） 已知其在SLE血清中升高。 将分离AL α IFN 通过亲和柱，由连接抗α IFN抗α IFN的琼脂糖组成， 身体 将比较AL α IFN和非酸不稳定α IFN。 因为它们对自然杀伤细胞功能的影响， B细胞功能和T细胞活化。 可能的直接参与 α干扰素在狼疮性肾炎免疫复合物病变中的作用 与各种其他慢性肾脏疾病平行的研究。 将通过以下方法测定α IFN的肾和皮肤组织沉积： 间接免疫荧光和α-干扰素与 测定免疫复合物或肾小球基底膜的成分。 将研究类风湿性关节炎患者的滑膜组织 对于α和γ IFN的产生和γ IFN释放的调节， 前列腺素E2检查，使用短期滑膜组织细胞培养。 从共培养的滑膜组织中释放的物质 可以诱导外周血单个核细胞产生IFN， 研究了 此外，内源性因子如抗淋巴细胞因子的作用也是重要的。 细胞抗体，推定的自身抗原（DNA，自体聚集的IgG， 核苷酸或核酸）刺激IFN释放的作用将是 考察 还将尝试确定α IFN 和γ-干扰素的产生与任何容易证明的 免疫控制机制 最后，将研究γ-干扰素的 对体外T和B细胞相互作用的可证实的作用。

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.