Prolactin: A Key Immunoregulator in Viral Infections and Autoimmune Diseases

Prolactin (PRL) is secreted by various cells in the anterior pituitary gland, mammary glands, placenta, uterus, ovaries, testes, skin, adipose tissue, endothelial cells, immune system, and central nervous system. The expression and secretion of PRL are influenced by several factors such as suckling, thyrotropin-releasing hormone (TRH), cytokines, dopamine, estrogen, and vasoactive intestinal polypeptide. It operates through a complex receptor, which is expressed in mammary gland cells, pancreatic beta cells, adipocytes, and immune cells. PRL is essential for various physiological functions, in particular milk production, breast development, metabolism, and immune regulation. Serum PRL levels fluctuate daily and can be affected by exercise, diet, and stress. Hyperprolactinemia is linked to autoimmune diseases and viral infections. In viral infections such as HIV, HCMV, HCV, and COVID-19, PRL levels are often increased, which may influence the immune responses. PRL can modulate the activity of various immune cells, including T cells, B cells, natural killer cells, and macrophages, mounting an effective immune response against viral infections. Moreover, PRL influences the production of cytokines that mediate and regulate immunity and inflammation. PRL stimulates B cells to produce antivirus antibodies that are essential for neutralizing viruses and preventing their spread within the body. PRL levels, varying by sex and life stage, may affect immune responses and susceptibility to viral infections. Moreover, overexpression of PRL was indicated in various autoimmune diseases. Overall, PRL is a complex hormone with significant implications for endocrine function, immune regulation, and immune responses to viral infections, highlighting the need for further research into its diverse roles in health and disease. This review summarizes current knowledge of the immunomodulatory effects of PRL in human viral infections and possibly its contribution to the development of autoimmune diseases.