INTERACTIONS OF CELLULAR AND HUMORAL IMMUNITY

细胞免疫和体液免疫的相互作用

• 批准号: 3154790
• 负责人: RALPH C WILLIAMS
• 金额: $ 13.65万
• 依托单位: UNIVERSITY OF NEW MEXICO
• 依托单位国家: 美国
• 财政年份: 1977
• 资助国家: 美国
• 起止时间: 1977-01-01 至 1990-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3154790
• 关键词: B lymphocyte; T lymphocyte; antirheumatic agents; autoimmune disorder; cell cell interaction; cellular immunity; choroid uvea; enzyme linked immunosorbent assay; gold; human subject; human tissue; humoral immunity; hybridomas; immune adherence reaction; immunization; immunofluorescence technique; immunoglobulin G; immunoglobulin M; immunologic assay /test; immunoregulation; liver disorder; mixed tissue /cell culture; monoclonal antibody; pregnancy immunology; radiation sensitivity; radioimmunoassay; radiotracer; renal toxin; rheumatic fever; rheumatoid arthritis; suppressor T lymphocyte; surface antigens; systemic lupus erythematosus; umbilical cord

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.

研究计划干扰素（IFNS）在modu- 1中的可能作用