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Research Article Free access | 10.1172/JCI116425

Interferon-gamma inhibits macrophage apolipoprotein E production by posttranslational mechanisms.

K Brand, N Mackman, and L K Curtiss

Department of Immunology, Scripps Research Institute, La Jolla, California 92037.

Find articles by Brand, K. in: PubMed | Google Scholar

Department of Immunology, Scripps Research Institute, La Jolla, California 92037.

Find articles by Mackman, N. in: PubMed | Google Scholar

Department of Immunology, Scripps Research Institute, La Jolla, California 92037.

Find articles by Curtiss, L. in: PubMed | Google Scholar

Published May 1, 1993 - More info

Published in Volume 91, Issue 5 on May 1, 1993
J Clin Invest. 1993;91(5):2031–2039. https://doi.org/10.1172/JCI116425.
© 1993 The American Society for Clinical Investigation
Published May 1, 1993 - Version history
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Abstract

Macrophage-derived apolipoprotein (apo) E and multimers of a synthetic apo E-peptide display monokine-like functions by inhibiting mitogen- or antigen-driven lymphocyte proliferation. This study demonstrated how the target lymphocyte itself can modulate macrophage apo E production. The lymphokine interferon-gamma (IFN) dramatically inhibited the accumulation of apo E in the supernatant of human monocytic THP-1 cells when present during phorbol myristate acetate-induced differentiation. A similar effect was observed when IFN was added to differentiated THP-1 cells. Treatment with IFN did not change the steady-state levels of apo E mRNA. Furthermore, in the presence of IFN no increased degradation or increased uptake of extracellular apo E was detected. Pulse-chase experiments indicated that IFN reduced the accumulation of extracellular apo E and increased the degradation of intracellular apo E. The inhibitory effect of IFN on apo E production also was observed in human monocyte-derived macrophages. Thus, our data demonstrated that IFN inhibited macrophage apo E production by posttranslational mechanisms. This represents a previously uncharacterized immunoregulatory interaction and lends further support to a relationship between lipid metabolism and the immune system.

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