I appreciate the opportunity to talk about
"The Pathogenic Role of Prolactin in Systemic Lupus Erythematosus".
In 1992, our question was,
does prolactin have a role in the pathogenesis of systemic lupus erythematosus, SLE?
In this editorial, taking together the clinical and experimental evidence at that time,
we supported the hypothesis that prolactin had
a role in the pathogenesis and clinical manifestations of SLE.
However, during these years,
the data implicating prolactin initially were largely circumstantial.
Now, in 2018, progress has been made in
the understanding the role of prolactin in
the pathogenesis of SLE and other hormonal diseases.
In fact, alteration of prolactin and sex hormones
can break immune tolerance and exacerbate easily.
Here, we propose that prolactin participate in
the pathogenesis of SLE interacting with innate,
and adaptive immune response.
In humans, prolactin gene is expressed on chromosome 6,
and is not restricted to the pituitary,
but occurs at multiples extra-pituitary sites such as endometrium,
myometrium, endothelial, epithelial, immune cells, etc.
Where it is under tissue specific control,
these tissues and cells are important targets in SLE and other hormonal diseases.
Tissues and cells of the human immune system expresses the prolactin gene.
The expression of prolactin mRNA in normal and normal human lymphoid tissues also observed in thymus,
spleen, tonsil, lymphoid nodes, and lymphoid thymus.
Prolactin mRNA was localized in lymphocytes,
epithelial cells, and vascular endothelial cells.