Prolactin (PRL) enhances inflammatory and antitumor responses in vitro and
thus exhibits Th1-type cytokine-like effects. Evidence from experimental mo
dels indicates that inhibition of PRL release by bromocriptine downregulate
s immune reactions and ameliorates autoimmune diseases in which Th1 respons
es are predominant. A direct effect of locally produced PRL in some Th1 dis
eases, such as rheumatoid arthritis, supports this concept. Paradoxically,
however, hyperprolactinemia can also be associated with conditions such as
pregnancy, where remission of Th1-mediated diseases is known to occur in th
e context of a Th2-dominated milieu. This reversal of the Th1-promoting eff
ect of PRL may be due to major changes in the levels of other hormones that
can annul and/or override the PRL-mediated proinflammatory state. Neverthe
less, PRL, as an immunopotentiating agent, may have a powerful therapeutic
role in cancer and other immunocompromised patients. (C) 2000 Elsevier Scie
nce B.V. All rights reserved.