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  • 标题:Intercellular adhesion molecule-1 inhibits interleukin 4 production by naive T cells
  • 本地全文:下载
  • 作者:Claudia R. Luksch ; Ola Winqvist ; Minette E. Ozaki
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:1999
  • 卷号:96
  • 期号:6
  • 页码:3023-3028
  • DOI:10.1073/pnas.96.6.3023
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:The type of cytokines produced during T cell responses determines susceptibility or resistance to many pathogens and influences the development of autoimmunity and allergy. To define the role of individual accessory molecules in cytokine production during primary immune responses, Drosophila cell lines expressing murine major histocompatibility complex class II molecules with defined combinations of accessory molecules were used to present peptide antigen to naive T cell receptor transgenic T cells. Significantly, expression of B7.1 or B7.2 without additional accessory molecules led to very high production of interleukin (IL)-4, which contrasted with minimal IL-4 production elicited by conventional antigen presenting cells (APC). However, coexpression of ICAM-1 and B7 on Drosophila APC induced little IL-4, suggesting an inhibitory role for intercellular adhesion molecule-1 (ICAM-1). In support of this idea, stimulation of T cell receptor transgenic T cells with peptide presented by splenic APC devoid of ICAM-1 (from ICAM-1-deficient mice) led to high IL-4 production. Thus, the level of IL-4 production by naive CD4+ T cells during typical primary responses appears to be controlled, at least in part, by T-APC interactions involving ICAM-1.
  • 关键词:cytokines ; B7 ; Drosophila antigen-presenting cell
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