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Interleukin 1 Secretion by Human Monocytes and Macrophages
Author(s) -
Mayernik David G.,
Haq Amin,
Rinehart John J.
Publication year - 1984
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.36.4.551
Subject(s) - monokine , biology , secretion , macrophage , macrophage activating factor , thymocyte , monocyte , cell culture , concanavalin a , t cell , immunology , microbiology and biotechnology , in vitro , interleukin , cytokine , immune system , endocrinology , biochemistry , genetics
Interleukin 1 (IL‐1) is generally regarded as a major regulator of T lymphocyte proliferation. Macrophages from animals and cloned tumor cell lines have been shown to produce this monokine in response to a variety of stimuli. The ability of human monocytes and macrophages to generate IL‐1 is much less well characterized. We previously demonstrated that human monocytes cultured for 1–6 days transformed to macrophages but retained their capacity to support concanavalin A‐driven T cell proliferation. However, cultured macrophage capacity to support antigen‐driven T cell proliferation began to decline after 3 days of culture and was markedly deficient by 6 days of culture. To determine if this loss of accessory cell function was due to the inability to secrete IL‐1, we measured the monokine produced by normal fresh human monocytes and macrophages cultured in vitro from monocytes. IL‐1 was assayed by the mouse thymocyte proliferation method. Fresh monocytes secreted IL‐1 readily in response to lipopolysaccaride and latex particles. Macrophages cultured from fresh monocytes, however, lost this ability after ≥2 days in culture. Mixing experiments failed to demonstrate an inhibitor present in the macrophage supernatants that would suppress thymocyte proliferation. Stimulated T cells incubated with monocytes and 3‐day cultured macrophages failed to prolong or promote IL‐1 secretion.