<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Neidhart M</dc:creator>
  <dc:creator>Gay RE</dc:creator>
  <dc:creator>Gay S</dc:creator>
  <dc:date>1999</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">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.</dc:description>
  <dc:identifier>https://sonar.ch/global/documents/55243</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/S0753-3322(99)80091-2</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/10424242</dc:relation>
  <dc:source>Biomedicine &amp; pharmacotherapy = Biomedecine &amp; pharmacotherapie. - 1999</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Animals</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Arthritis, Rheumatoid</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Humans</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Hyperprolactinemia</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Peptides</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Prolactin</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Risk Factors</dc:subject>
  <dc:title xmlns:ns8="xml" ns8:lang="en">Prolactin and prolactin-like polypeptides in rheumatoid arthritis.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
