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  • 标题:Ligation of major histocompatibility complex class II molecules mediates apoptotic cell death in resting B lymphocytes
  • 本地全文:下载
  • 作者:M K Newell ; J VanderWall ; K S Beard
  • 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:1993
  • 卷号:90
  • 期号:22
  • 页码:10459-10463
  • DOI:10.1073/pnas.90.22.10459
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:Class II major histocompatibility complex-encoded molecules expressed on the surface of primed B lymphocytes function as restriction elements for presentation of antigen to T lymphocytes, an interaction that ultimately leads to activation and differentiation of both cell types. The engagement of class II on a resting B cell, on the other hand, inhibits subsequent B-cell growth and activation. Our studies show that treatment of resting B lymphocytes with anti-class II antibodies, or with other agents (dibutyryl cAMP or isoproterenol) that increase intracellular levels of cAMP, results in the apoptotic death of most or all of the resting B cells. Conversely, treating cells with immobilized anti-immunoglobulin and interleukin 4, conditions known to prime cells, protects them from class II-mediated death and specifically from increases in nucleosomal fragments characteristic of apoptotic death. Freshly ex vivo activated B cells likewise are refractory to class II-mediated apoptosis. Treating B cells with anti-class II reagents causes an elevation of cAMP in resting, but not in activated, B cells. These results suggest that apoptotic death is a mechanism of prevention of nonspecific B-cell activation in the event that T-cell receptor and/or CD4 ligation of major histocompatibility complex class II occurs in the absence of antigen.
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