Open AccessDifferential augmentation of in vivo natural killer cytotoxicity in normal primates with recombinant human interleukin‐1 and granulocyte‐macrophage colony‐stimulating factor
Author(s) -
DAVIS T. A.,
MONROY R. L.,
SKELLY R. R.,
DONAHUE R. E.,
MACVITTIE T. J.
Publication year - 1990
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1990.tb08108.x
Subject(s) - granulocyte macrophage colony stimulating factor , in vivo , immunology , granulocyte , natural killer cell , cytokine , stimulation , biology , interleukin , medicine , colony stimulating factor , granulocyte colony stimulating factor , endocrinology , in vitro , cytotoxicity , chemotherapy , haematopoiesis , biochemistry , microbiology and biotechnology , genetics , stem cell
SUMMARY The effect of recombinant human interleukin‐1 (IL‐1) alpha, granulocyte‐macrophage colony‐stimulating factor (GM‐CSF), and combined factor therapy (CFT) on Rhesus monkey peripheral blood natural killer (NK) activity in vivo was compared. During a 14‐day treatment period, IL‐1‐treated animals demonstrated a 170% increase in NK activity against K562 target cells by day 4 , reaching maximal levels (300%) at day 16 , and returning to baseline by day 30. NK activity of GM‐CSF‐treated monkeys increased slightly (60–100%) during days 4–12. as did saline‐treated monkeys, but returned to baseline values by day 16. A delayed increase in NK activity resulted after GM‐CSF treatment, reaching a peak (260%) on day 23 and remaining elevated through day 39. CFT resulted in a bimodal response pattern, with two peaks of NK activity, one at day 16 and a second at day 39 , The first peak of activity (223%) was significantly less than the activity attained with IL‐1 alone; the second peak (300%) was of greater duration and occurred later than the peak observed in GM‐CSF‐treated monkeys. Unlike IL‐1, GM‐CSF treatment did not lead to a immediate stimulation of NK activity; augmentation was delayed by more than 7 days post treatment. CFT results suggest that GM‐CSF reduced the direct NK response to IL‐1; while IL‐1 led to an enhanced delayed NK response. Therefore, IL‐1 and GM‐CSF augment NK activity through different but interrelated pathways.