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The cell lines FDC-Pl and 32D cl-23 have previously been used as unique indicators for the growth-promoting activity of interleukin-3. We show that FDC-Pl cells respond to granulocyte/macrophage colony-stimulating factor (GM-CSF. CSF-2) as well as to interleukin-3. In keeping with this finding, FDC-Pl cells express the macrophage-specific marker, F4/80. FDC-Pl cells do not, however, respond to macrophage CSF (M-CSF, CSF-1). In contrast, 32D cl-23 cells do not respond to GM-CSF and lack F4/80. Instead, 32D cl-23 cells respond to an as yet undefined factor in conditioned medium (CM) from the primate T cell line, MLA-144, and CM from mitogen-stimulated human lymphocytes (HLCM). 32D cl-23 cells are Lyt-1+. Both FDC-Pl and 32D cl-23 cells consume interleukin-3, but only FDC PI cells consume GM-CSF. Similarly, 32D cl-23, but not FDC-Pl, cells consume 32D cl-23 growth factor from MLA-144 CM and HLCM. lnterleukin-3-dependent cell lines must therefore concurrently express different functional cell surface receptors for a variety of biochemically distinct growth factors.

Adherent monolayer cultures of human blood monocytes, peritoneal macrophages, bone marrow macrophages, and colonic mucosa macrophages were examined for their ability to produce and secrete minactivin, a specific inactivator of urokinase-type plasminogen activator. All except colonic mucosa macrophages produced and secreted appreciable amounts of minactivin, but only blood monocytes were stimulated by muramyl dipeptide (adjuvant peptide) to increase production. The minactivin from each of these populations could be shown to preferentially inhibit urokinase-type plasminogen activator and not trypsin, plasmin, or “tissue “-type plasminogen activator (HPA66). A plasminogen-activating enzyme present in monocyte cultures appeared unaffected by the presence of minactivin and could be shown to be regulated independently by dexamethasone.