Prolactin and Autoimmunity |
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Authors: | Email author" target="_blank">Annamaria?De?BellisEmail author Antonio?Bizzarro Rosario?Pivonello Gaetano?Lombardi Antonio?Bellastella |
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Institution: | (1) Department of Clinical and Experimental Medicine and Surgery “F. Magrassi, A. Lanzara”, Second University of Naples, via Pansini N. 5, 80131 Napoli, Italy;(2) Department of Molecular and Clinical Endocrinology and Oncology. “Federico II”, University of Naples, Italy |
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Abstract: | The interrelationship between prolactin (PRL) and the immune system have been elucitaded in the last decade, opening new important
horizons in the field of the immunoendocrinology. PRL is secreted not only by anterior pituitary gland but also by many extrapituitary
sites including the immune cells. The endocrine/paracrine PRL has been shown to stimulate the immune cells by binding to PRL
receptors. Increased PRL levels, frequently described in autoimmune diseases, could depend on the enhancement of coordinated
bi-directional communications between PRL and the immune system observed in these diseases. Hyperprolactinemia has been described
in the active phase of some non organ-specific autoimmune diseases, as systemic lupus erythematosus (SLE) and rheumatoid arthritis
(RA) and organ-specific autoimmune diseases, as celiac disease, type 1 diabetes mellitus, Addison's disease, autoimmune thyroid
diseases. In these diseases PRL increases the syntesis of IFNγ and IL-2 by Th1 lymphocytes. Moreover, PRL activates Th2 lymphocytes
with autoantibody production. Of particular interest is the association between hyperprolactinemia and levels of anti DNA
antibodies, islet cell antibodies (ICA), thyreoglobulin antibodies (TgAb), thyroperoxidase antibodies (TPOAb), adrenocortical
antibodies (ACA), transglutaminase antibodies (tTGAb) in SLE, in type 1 diabetes mellitus, in Hashimoto's thyroiditis, in
Addison's disease and in celiac disease, respectively. High levels of PRL have been also frequently detected in patients with
lymphocytic hypophysitis (LYH). Several mechanisms have been invoked to explain the hyperprolactinemia in LYH. The PRL increase
could be secondary to the inflammatory process of the pituitary gland but, on the other hand, this increase could have a role
in enhancing the activity of the immune process in LYH. Moreover, the detection of antipituitary antibodies targeting PRL-secreting
cells in some patients with idiopathic hyperprolactinemia suggests the occurrence of a possible silent LYH in these patients.
Finally, the role of anti-prolactinemic drugs to inactivate the immune process in LYH is still discussed. |
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Keywords: | prolactin antipituitary antibodies lymphocytic hypophysitis autoimmune diseases |
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