PROLACTIN IS AN AUTOCRINE GROWTH-FACTOR FOR THE JURKAT HUMAN T-LEUKEMIC CELL-LINE

Despite convincing evidence of cooperation between IL-2 and endogenous prolactin (PRL) during T cell activation, the individual role of PRL as a T-cell lineage cytokine remains to be defined. We have examined t he production and function of PRL on the Jurkat human T-leukemic cell line, which does not constitutively produce IL-2. The majority of Jurk at cells expressed PRL receptor (R) under standard culture conditions, whereas appearance of the a chain of the IL-2-R required PHA-PMA stim ulation, as did IL-2 synthesis. Western blotting revealed a predominan t band at 23.5 kDa and a weaker band at 25.5 kDa in both Jurkat cell l ysates and human (h) pituitary PRL. Metabolic labeling of the cell lys ates with S-35-methionine and immunoprecipitation with an antiserum ag ainst hPRL showed that both forms of PRL are actively synthesized by t he Jurkat cell line. PRL released in the medium was biologically activ e in the rat Nb2 lymphoma mitogenic assay. Depletion of medium PRL wit h two polyclonal anti-hPRL antisera inhibited the growth of Jurkat cel ls in a dose-dependent manner, as evaluated by cell number and H-3-TdR uptake. Purified pituitary or recombinant hPRL at a wide range of con centrations had no significant effect on their growth, but reversed th e blocking activity of the anti-hPRL antibody, Recombinant IL-2 had no effect on the antibody-induced growth inhibition. Taken as a whole, t hese results demonstrate that PRL can act as an autocrine T cell growt h factor independently of IL-2 and are the first evidence of its invol vement in human leukemic growth and possibly in leukemic transformatio n. (C) 1997 Elsevier Science B.V.