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Prolactin in autoimmune diseases

M Neidhart1

  • 1Department of Rheumatology, University Hospital, Zürich, Switzerland.

Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.)
|April 1, 1998
PubMed
Summary

Prolactin (Prl), a hormone traditionally linked to lactation, plays a significant role in the immune system. Mild hyperprolactinemia may increase the risk of developing autoimmune diseases like lupus and diabetes.

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Area of Science:

  • Neuroendocrinology
  • Immunology
  • Endocrinology

Background:

  • Prolactin (Prl) is traditionally viewed as a lactogenic hormone, but its role in immunity is increasingly recognized.
  • Prl and Prl-like peptides can be produced by immune cells and fibroblasts, not just the pituitary gland.
  • Elevated Prl levels are observed in various autoimmune conditions, including arthritis, lupus erythematosus (SLE), and type I diabetes.

Purpose of the Study:

  • To explore the emerging role of prolactin (Prl) in immune system regulation and autoimmune diseases.
  • To investigate the connection between hyperprolactinemia and the development of autoimmunity.
  • To highlight Prl as a potential link between the neuroendocrine and immune systems.

Main Methods:

  • Literature review and synthesis of existing research on prolactin and autoimmunity.
  • Analysis of studies reporting elevated Prl levels in animal models and human autoimmune diseases.
  • Discussion of the proposed mechanisms by which Prl influences immune responses, such as promoting anti-dsDNA production in SLE.

Main Results:

  • Mild hyperprolactinemia is suggested as a risk factor for autoimmunity, occurring in conditions like postpartum or adrenocortical deficiency.
  • In human SLE, Prl may enhance the production of anti-double stranded DNA antibodies.
  • Prolactin acts as a stimulatory link between the neuroendocrine and immune systems, contrasting with the immune-dampening effects of glucocorticoids.

Conclusions:

  • Prolactin's role extends beyond lactation, significantly impacting immune function and autoimmune disease development.
  • Further research into Prl-inhibiting therapies for SLE, considering genetic factors like HLA-DRB1*0301, is warranted.
  • Investigating extra-pituitary Prl-like cytokines and their role in conditions like rheumatoid arthritis is a key future direction.

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