Abstract
IT is more than thirty years since Billingham and Medawar showed that adrenocorticotrophic hormone (ACTH) and cortisol can prolong the survival of skin allografts1,2. It has since become clear that glucocorticoid hormones are critically involved in the regulation of immunity3,4. The level of glucocorticoids secreted in response to antigenic challenge corresponds to the magnitude of the immune response and in general reaches immunosuppressive levels5–7. Interestingly, not all immune responses enhance ACTH and glucocorticoid hormone production. In transplantation immunity, the reverse seems to be true: circulating glucocorticoid levels at the time of skin graft rejection are lower than control levels8. Because β-endorphin and ACTH originate from the same prohormone, pro-opiomelanocortin (POMC)9, and are closely related in their tissue-specific processing and coordinate release10–12, we have investigated the role of pituitary β-endorphin in transplantation immunity. We report here that POMC biosynthesis and processing in the pars intermedia, but not in the anterior pituitary, can be regulated by T cell-specific factors secreted in animals undergoing transplantation immunity.
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Zakarian, S., Eleazar, M. & Silvers, W. Regulation of pro-opiomelanocortin biosynthesis and processing by transplantation immunity. Nature 339, 553–556 (1989). https://doi.org/10.1038/339553a0
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DOI: https://doi.org/10.1038/339553a0
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