Ciclosporin has been demonstrated to inhibit prolactin binding to lymphocyte prolactin receptors and inhibit prolactin-stimulated ornithine decarboxylase (ODC) activity in kidney, liver, spleen, thymus, heart, adrenal, and aorta. Urinary polyamine excretion studies in ciclosporin-immunosuppressed patients provided clinical evidence that the polyamine biosynthetic pathway, where ODC is the initial enzyme, was being inhibited by ciclosporin therapy. A requirement for prolactin in the regulation of immune responses has been demonstrated and we report evidence indicating that one possible mechanism of immunosuppressive activity of ciclosporin at therapeutic concentrations may be through specific blockade of the lymphocyte prolactin receptor. However, at ciclosporin concentrations considered to be subimmunosuppressive, ciclosporin consistently enhanced the binding of (125I)-prolactin to human lymphocytes and also potentiated the induction of prolactin-stimulated ODC in the kidney, spleen and thymus. In addition, neuroendocrine regulation of the immune response through episodic release of prolactin was detected prior to allograft rejection in ciclosporin-immunosuppressed patients and may be a key event leading to allograft rejection in the ciclosporin-immunosuppressed patient.
|Original language||English (US)|
|Number of pages||17|
|Journal||Progress in Allergy|
|Publication status||Published - 1986|
ASJC Scopus subject areas
- Immunology and Allergy