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Blood, Vol. 92 No. 11 (December 1), 1998:
pp. 4353-4365
Autocrine Signals Control CCAAT/Enhancer Binding Protein
 Expression, Localization, and Activity in Macrophages
Mark Baer,
Simon C. Williams,
Allan Dillner,
Richard C. Schwartz, and
Peter F. Johnson
From the ABL-Basic Research Program, National Cancer
Institute-Frederick Cancer Research and Development Center, Frederick,
MD; and the Department of Microbiology, Michigan State University, East
Lansing.
The transcription factor CCAAT/enhancer binding protein  (C/EBP, or NF-IL6) is expressed in macrophages, where it
participates in lipopolysaccharide (LPS)-mediated induction of
proinflammatory cytokine genes such as interleukin-6 (IL-6) and
IL-1. We have identified activities in conditioned medium from a
macrophage tumor cell line that regulates the expression, localization,
and transcriptional activity of C/EBP. One factor was shown to be tumor necrosis factor- (TNF-), which increased C/EBP
expression by a posttranscriptional mechanism. A second activity,
designated autocrine macrophage factor (AMF), elicited a change in
C/EBP localization from a punctate nuclear staining pattern to
diffuse nuclear distribution. The punctate form of C/EBP correlated
with increased susceptibility of this protein to cleavage by an
endogenous protease during nuclear extract preparation. Conditioned
medium stimulated the ability of C/EBP to transactivate a reporter
gene and activated the expression of two cytokine genes that are
putative targets of C/EBP. These observations suggest that diffuse
distribution of C/EBP in the nucleus corresponds to an activated
form of this protein. AMF activity could not be mimicked by an
extensive set of recombinant cytokines and growth factors and therefore
may represent a novel extracellular factor.
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