Prolactin, a link between neuroendocrine and immune system. Its role in the pathogenesis of rheumatic diseases

M. A. Gutierrez, J. M. Anaya, G. E. Cabrera, O. Vindrola, L. R. Espinoza

Resultado de la investigación: Contribución a una revistaArtículo de revisiónrevisión exhaustiva

4 Citas (Scopus)

Resumen

Increasing evidence suggest that prolactin (PRL) has important immunoregulatory properties and may play a role in the pathogenesis and disease expression of certain autoimmune diseases. Prolactin is co-mitogenic on murine and human lymphocytes, induces the formation of IL-2 cell surface receptor and modulates the expression of various growth factor related genes. Prolactin also stimulates antibody production both in vivo and in vitro. Specific high affinity prolactin-receptors have been described on T and B lymphocytes as well as on monocytes. They are distributed on heterogeneous lymphocyte subsets and they showed imbalance in autoimmune situations. Lymphocytes may produce PRL-like proteins biologically active that function as autocrine growth factors for lymphoproliferation. Hyperprolactinemia has been found in male patients with systemic lupus erythematosus (SLE) and also during pregnancy in SLE patients. Hyperprolactinemia is correlated with clinical and serological activity in a subset of SLE patients. High levels of PRL aggravates disease activity and accelerates mortality in the B/W mouse model of SLE. In rheumatoid arthritis an excessive and upregulated secretion of PRL has been shown. Hyperprolactinemia has also been shown in a subset of patients with primary Sjogren's syndrome. High PRL levels have been found in Reiter's syndrome patients and bromocriptine treatment has been reported effective in these patients and psoriatic arthritis patients. These data support a potential role of this immunoregulatory hormone in the pathogenesis of some rheumatic diseases.

Idioma originalInglés estadounidense
Páginas (desde-hasta)261-267
Número de páginas7
PublicaciónRevue du Rhumatisme (English Edition)
Volumen61
N.º4
EstadoPublicada - 1994
Publicado de forma externa

All Science Journal Classification (ASJC) codes

  • Reumatología

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