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.
