Journal article
Prolactin and prolactin-like polypeptides in rheumatoid arthritis.
- Neidhart M WHO Collaborating Center for Molecular Biology, University Hospital, Zürich, Switzerland.
- Gay RE
- Gay S
- 1999-07-29
Published in:
- Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. - 1999
English
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.
- Language
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- English
- Open access status
- closed
- Identifiers
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- DOI 10.1016/S0753-3322(99)80091-2
- PMID 10424242
- Persistent URL
- https://sonar.ch/global/documents/55243
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