In this review, the authors attempt to provide a critical overview on the role of prolactin in the immune system, exploring its contribution to the development of autoimmune diseases.
Concentration-dependent effects of estrogen on the immune system; the role of progesterone, androgens, leptin, oxytocin, and prolactin; and the interplay between Th1 and Th2 immune responses together maintain a delicate balance between host defense, immunological tolerance and autoimmunity.
Prolactin (PRL), an inflammatory hormone with cytokine properties, has long been proposed to play a crucial role in the pathogenesis of autoimmune disorders, including rheumatoid arthritis (RA).
Thus, hyperprolactinemia case with serum prolactin level >100 ng/mL may require long-term follow-up for the development of autoimmune disease in future.
Human prolactin (PRL) is a well-known hormone for pituitary of lactation and reproduction, but it also has immunostimulatory effect in some inflammatory or autoimmune diseases including psoriasis, which has not been well elucidated.
High levels of prolactin may lead either to the development of autoimmune diseases in susceptible mothers or exacerbations of current immune-mediated disorders.
Anti-PIT-1 antibody syndrome has recently been reported and characterized by acquired growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone (TSH) deficiencies associated with autoimmunity to a pituitary specific transcription factor PIT-1, which plays an essential role in GH-, PRL-, and TSH-producing cells.
PRL levels have been investigated in several autoimmune diseases including systemic lupus erythematosus (SLE), however, yielded different and inconsistent results.
PRL stimulates B and T lymphocyte proliferation, and its excess is associated with the appearance or recrudescence of various systemic and organ-specific autoimmune diseases, as demonstrated by experimental studies performed in mice, and by human case reports and case control studies.
PRL levels have been investigated in several autoimmune diseases including multiple sclerosis (MS); however, these have yielded different and inconsistent results.
Increased levels of prolactin (PRL) have recently been associated with carcinogenesis and the exacerbation of autoimmune diseases, and might be involved in the progression of tuberculosis (TB).
Recent studies demonstrate that prolactin impairs all three mechanisms of B cell tolerance induction (negative selection, receptor editing, and anergy) and thereby contributes to the pathogenesis of autoimmunity.
Further studies are necessary to elucidate the mechanisms by which prolactin affects autoimmune disease activity, increase the inflammatory mechanism, and determine the role of anti-prolactinemic drugs to regulate the immune/inflammatory process.
PRL has an immunostimulatory effect and promotes autoimmunity: PRL impairs the negative selection of autoreactive B lymphocytes occurring during B cell maturation into fully functional B cells.