Prolactin and prolactin-like polypeptides in rheumatoid arthritis.
A bidirectional communication network exists between the neuroendocrine and immune systems, and a dysfunctional communication may contribute to the development of autoimmune diseases in various species, including humans. Experimental, epidemiological, and clinical data suggest that breast feeding and hyperprolactinemia constitute a risk factor for the development of diseases with autoimmune components, including rheumatoid arthritis (RA). We hypothesized that the anterior pituitary hormone prolactin (Prl) and locally produced Prl-like polypeptides may act as endocrine, autocrine, and paracrine regulators of synovial cell functions. They may participate not only in enhancing T-lymphocyte immune reactivity, but also in the exacerbation of RA lesions through their influence on synovial fibroblasts. In RA synovial tissue, Prl-like polypeptides could participate in a bidirectional communication between immunocytes and fibroblasts. Both Prl and Prl-like polypeptides might act via proto-oncogenes and transcriptional factors, leading to cell proliferation, i.e., synovial tissue hyperplasia, neo-angiogenesis, and the production of catabolic enzymes such as matrix metalloproteinases and cathepsins. In such cases, they could represent important regulators of the T-cell independent mechanism of joint destruction.
Neidhart
M
M
WHO Collaborating Center for Molecular Biology, University Hospital, Zürich, Switzerland.
Gay
R E
RE
Gay
S
S
D000818:Animals; D001172:Arthritis, Rheumatoid / Q000209:etiology*; D006801:Humans; D006966:Hyperprolactinemia / Q000150:complications; D010455:Peptides / Q000502:physiology*; D011388:Prolactin / Q000502:physiology*; D012307:Risk Factors
D010455:Peptides; D011388:Prolactin