PROLACTIN IN AUTOIMMUNE-DISEASES

The immune system is still regarded by many as autonomous, and prolact in (Prl) has traditionally been considered as a lactogenic hormone. Ov er the last 10 years, the total number of publications considering Prl is decreasing, while the number of those investigating its role in im munity sustainly increased. In addition to the pituitary gland, Prl-li ke peptides can be produced by activated leukocytes and fibroblasts. E levated serum levels of Prl in (rat) adjuvant arthritis, (murine) coll agen type Il-induced arthritis, (murine and human) systemic lupus eryt hematosus (SLE), and (murine and rat) autoimmune type I diabetes may i nfluence the outcome of the disease. It is suggested that mild hyperpr olactinemia is a risk factor for the development of autoimmunity. This can occur under certain circumstances, for example adrenocortical def iciency or postpartum. In human SLE, Prl appears to favor the producti on of anti-double stranded DNA. While glucocorticoids would damp the i mmune reactivity, Prl constitutes a stimulatory link between the neuro endocrine and immune systems. Future directions should include: 1) mul ticenter projects for evaluation of the therapy with Prl-inhibiting co mpounds in SLE, considering for example the HLA-DRB1 0301 status; and 2) the regulation of extra-pituitary Prl-like cytokines (''proliferin s'') (e.g., in rheumatoid arthritis synovium) and their role in the pr oduction of catabolic enzymes.