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：1989
卷号：86
期号：24
页码：10034-10038
DOI：10.1073/pnas.86.24.10034
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：To examine the effects of aberrant expression of class II major histocompatibility complex (MHC) proteins on tolerance development, transgenic mice expressing the I-Ad genes under control of the pancreatic elastase promoter were produced. Such transgenic mice express I-Ad exclusively on exocrine pancreas, without expression in thymus or by lymphocytes. No spontaneous development of autoimmune reactivity toward exocrine pancreas was found in transgene-expressing mice of an H-2b background even though such mice could produce in vitro allogeneic responses against I-Ad. When T cells from nontransgenic H-2b mice as well as transgenic H-2b mice were activated in vitro by I-Ad allogeneic stimulator cells and transferred to transgenic mice, an intense, destructive lymphocytic infiltrate specific for exocrine pancreas developed. These findings suggest that aberrant class II MHC expression alone may not trigger autoimmune reactions. Rather, the unresponsiveness to allogenic class II MHC may result from the inability of exocrine pancreas to initiate primary responses by T cells.
