De Bellis Annamaria, Bizzarro Antonio, Pivonello Rosario, Lombardi Gaetano, Bellastella Antonio
Department of Clinical and Experimental Medicine and Surgery F. Magrassi, A. Lanzara, Second University of Naples, via Pansini N. 5, 80131, Napoli, Italy.
Pituitary. 2005;8(1):25-30. doi: 10.1007/s11102-005-5082-5.
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 IFNgamma 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.
过去十年间，催乳素（PRL）与免疫系统之间的相互关系已被阐明，这为免疫内分泌学领域开辟了新的重要视野。PRL不仅由垂体前叶分泌，还由包括免疫细胞在内的许多垂体外部位分泌。内分泌/旁分泌型PRL已被证明可通过与PRL受体结合来刺激免疫细胞。自身免疫性疾病中经常出现的PRL水平升高，可能取决于这些疾病中PRL与免疫系统之间协同双向通讯的增强。高催乳素血症已在一些非器官特异性自身免疫性疾病（如系统性红斑狼疮（SLE）和类风湿性关节炎（RA））以及器官特异性自身免疫性疾病（如乳糜泻、1型糖尿病、艾迪生病、自身免疫性甲状腺疾病）的活动期被描述。在这些疾病中，PRL可增加Th1淋巴细胞产生IFNγ和IL-2。此外，PRL通过产生自身抗体激活Th2淋巴细胞。特别值得关注的是，高催乳素血症与SLE、1型糖尿病、桥本甲状腺炎、艾迪生病和乳糜泻中抗DNA抗体、胰岛细胞抗体（ICA）、甲状腺球蛋白抗体（TgAb）、甲状腺过氧化物酶抗体（TPOAb）、肾上腺皮质抗体（ACA）、转谷氨酰胺酶抗体（tTGAb）水平之间的关联。淋巴细胞性垂体炎（LYH）患者中也经常检测到高水平的PRL。人们提出了几种机制来解释LYH中的高催乳素血症。PRL升高可能继发于垂体的炎症过程，但另一方面，这种升高可能在增强LYH中免疫过程的活性方面发挥作用。此外，在一些特发性高催乳素血症患者中检测到针对分泌PRL细胞的抗垂体抗体，提示这些患者可能存在隐匿性LYH。最后，抗催乳素药物在使LYH中的免疫过程失活方面的作用仍在讨论中。
