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*
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan;
Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Osaka, Japan;
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston MA 02115; and
§
Mammalian Genetics Laboratory, Advanced BioScience Laboratories-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702
C-type lectins serve multiple functions through recognizing
carbohydrate chains. Here we report a novel C-type lectin,
macrophage-inducible C-type lectin (Mincle), as a downstream target of
NF-IL6 in macrophages. NF-IL6 belongs to the CCAAT/enhancer binding
protein (C/EBP) of transcription factors and plays a crucial role in
activated macrophages. However, what particular genes are regulated by
NF-IL6 has been poorly defined in macrophages. Identification of
downstream targets is required to elucidate the function of NF-IL6 in
more detail. To identify downstream genes of NF-IL6, we screened a
subtraction library constructed from wild-type and NF-IL6-deficient
peritoneal macrophages and isolated Mincle that exhibits the highest
homology to the members of group II C-type lectins. Mincle mRNA
expression was strongly induced in response to several inflammatory
stimuli, such as LPS, TNF-
, IL-6, and IFN-
in wild-type
macrophages. In contrast, NF-IL6-deficient macrophages displayed a much
lower level of Mincle mRNA induction following treatment with these
inflammatory reagents. The mouse Mincle proximal promoter region
contains an indispensable NF-IL6 binding element, demonstrating that
Mincle is a direct target of NF-IL6. The Mincle gene
locus was mapped at 0.6 centiMorgans proximal to CD4 on
mouse chromosome 6.
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