Effects of prolactin on cloned human T-lymphocytes.
To evaluate the possible role of prolactin (PRL) in T-lymphocytes, we monitored gene induction in one cytotoxic T-lymphocyte (CTL) clone derived from a patient with hemochromatosis and in several T-helper clones generated from a normal donor and a patient with multiple sclerosis. The CTL clone expressed conventional PRL receptor (PRLR), and PRL induced the expression of suppressor of cytokine signaling-3 (SOCS-3) and increased the expression of SOCS-2 and cytokine-inducible src homology-2 containing protein (CIS, another member of the SOCS family). As is the case in granulocytes, expression of a conventional receptor for PRL could not be shown by polymerase chain reaction analysis on three helper clones. In addition, as in granulocytes, PRL modulated the expression of genes such as the interferon-regulatory factor-1, inducible nitric oxide synthase, CIS, and SOCS-2. These effects were also elicited with ovine PRL and could be prevented by anti-PRL antibodies. Thus, the use of clones allowed the detection of direct effects of PRL on T-cells, even when these have few or no detectable PRLR, confirming that human T-lymphocytes are targets for PRL.
Dogusan
Zeynep
Z
Neuroendocrine Immunology Lab, Medical School, Free University of Brusssels (VUB), Belgium.
Martens
Nele
N
Stinissen
Piet
P
Hellings
Niels
N
Demotte
Nathalie
N
Hooghe
Robert
R
Hooghe-Peters
Elisabeth
E
D002999:Clone Cells; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D011388:Prolactin / Q000494:pharmacology*; D011981:Receptors, Prolactin / Q000235:genetics; D015398:Signal Transduction / Q000187:drug effects; D013601:T-Lymphocytes / Q000187:drug effects* / Q000502:physiology*; D015533:Transcriptional Activation
D011981:Receptors, Prolactin; D011388:Prolactin