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Human choriocarcinoma JAR cells constitutively express pro-interleukin-1beta that can be released with Fc(gamma)
J N Jarvis1, C Xu, L Zhao
1Division of Immunology/Rheumatology, Wayne State University, and the Children's Hospital of Michigan, Detroit 48201, USA.
Some authors have suggested that fetally derived syncytiotrophoblasts, which form the barrier between mother and the fetus, are an integral part of a complex macrophage-cytokine network involving maternal leukocytes, decidual cells, placental tissues, and even the fetus itself. We report here that syncytiotrophoblast-like JAR cells, a human choriocarcinoma cell line, share another feature common to cells of the monocyte-macrophage lineage, the ability to secrete IL-1beta when stimulated through their Fc(gamma) receptors. We incubated JAR cells with physiologically relevant concentrations of model BSA-rabbit IgG-anti-BSA immune complexes or monomeric rabbit IgG for periods of up to 72 h. Both monomeric IgG and immune complexes induced IL-1beta from JAR cells, although levels produced by immune complexes were approximately twice those induced by monomeric IgG. IL-1beta secretion was not inhibited by cycloheximide, and Western blots of JAR cell lysates using pro-IL-1beta MAb revealed constitutive expression of a 31-kD protein, whose levels declined within 2 h of stimulation by either IgG or immune complexes, but returned to baseline within 18 h.
Some authors have suggested that fetally derived syncytiotrophoblasts, which form the barrier between mother and the fetus, are an integral part of a complex macrophage-cytokine network involving maternal leukocytes, decidual cells, placental tissues, and even the fetus itself. We report here that syncytiotrophoblast-like JAR cells, a human choriocarcinoma cell line, share another feature common to cells of the monocyte-macrophage lineage, the ability to secrete IL-1beta when stimulated through their Fc(gamma) receptors. We incubated JAR cells with physiologically relevant concentrations of model BSA-rabbit IgG-anti-BSA immune complexes or monomeric rabbit IgG for periods of up to 72 h. Both monomeric IgG and immune complexes induced IL-1beta from JAR cells, although levels produced by immune complexes were approximately twice those induced by monomeric IgG. IL-1beta secretion was not inhibited by cycloheximide, and Western blots of JAR cell lysates using pro-IL-1beta MAb revealed constitutive expression of a 31-kD protein, whose levels declined within 2 h of stimulation by either IgG or immune complexes, but returned to baseline within 18 h.