Interleukin-2 apparently upregulates its receptor and induces proliferation of various resting mononuclear leukocytes in the absence of antigen.
We demonstrate that exposure to highly purified recombinant interleukin 2 (rIL-2) in the absence of known antigenic stimulation induces/increases the expression of two activation-associated proteins, the interleukin 2 receptor (IL-2R) and 4F2 on "resting" peripheral blood mononuclear cells (PBMC); subsequently, these cells enter the S phase of the cell cycle and proliferate. Dual parameter flow cytometry indicates that the phenotype of the cell population(s) which proliferate following this treatment includes HNK+, DR+, and T3+ cells. A twofold expansion in the number of HNK+ and DR+ cells was observed upon culturing resting PBMC in rIL-2 over a 6-day culture period. While the HNK monoclonal antibody is not specific for NK cells, these data do suggest that antigen independent growth of HNK+ cells may represent an additional mechanism by which IL-2 enhances NK effector activity, i.e., by induction of clonal growth of NK cells. In contrast, several concentrations of recombinant Interferon-gamma failed to produce a similar proliferative response.
D002469:Cell Separation; D002478:Cells, Cultured; D005434:Flow Cytometry; D006801:Humans; D007376:Interleukin-2 / Q000494:pharmacology*; D008213:Lymphocyte Activation / Q000187:drug effects*; D008214:Lymphocytes / Q000187:drug effects*; D011971:Receptors, Immunologic / Q000187:drug effects*; D015375:Receptors, Interleukin-2
D007376:Interleukin-2; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2