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Title 

Impaired responses of leukemic dendritic cells derived from a human myeloid cell line to LPS stimulation

Authors 

Kwang Dong KimSeung-Chul ChoiYoung Woock NohJ W KimS G PaikY YangK I KimJ S Lim

Publisher 

Korean Society of Medical Biochemistry

Issue Date 

2006

Citation 

Experimental and Molecular Medicine, vol. 38, no. 1, pp. 72-84

Keywords 

antigens, CD40cell differentiationdendritic cellskiller cells, naturallipopolysaccharidestoll-like receptorsB7 antigenCD40 antigenCD83 antigenCD86 antigen

Abstract 

Several myeloid leukemia-derived cells have been reported to possess the ability to differentiate into dendritic cells (DC). MUTZ-3, a myeloid leukemia cell line, responds to GM-CSF, IL-4 and TNF-α, and acquires a phenotype similar to immature monocyte-derived DC (MoDC). In the present study, MUTZ-3-derived DC (MuDC) showed high level expression of HLA class II molecules, CD80 and CD86, and were able to function as potent antigen presenting cells as previously reported. Interestingly, MuDC maturation was induced by CD40-mediated stimulation, but not by LPS stimulation. We analyzed CCR1, CCR7 and Toll-like receptor (TLR) expressions in MuDC, and measured IL-10 and IL-12 production after maturation stimuli. Although MuDC expressed the mRNA for TLR4, a major component of the LPS receptor system, they did not show an enhanced level of CCR7 or cytokine production after LPS stimulation. In contrast, they responded to CD40 stimulation, which resulted in increased levels of CD83, CD86 and CCR7. Moreover, while LPS-stimulated MoDC could potently stimulate NK cells in a DC-NK cell co-culture, LPS-stimulated MuDC failed to stimulate primary NK cells. Taken together, our findings suggest that, although MuDC express TLR4, unlike TNF-α and IL-1β, LPS does not stimulate MuDC to acquire mature phenotypes, and they may have impaired activity to initiate innate immune response.

ISSN 

1226-3613

Link 

http://dx.doi.org/10.1038/emm.2006.9

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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