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

Authors
Kim, KDChoi, SCNoh, YWKim, JWPaik, SGYang, YKim, KILim, JS
Issue Date
Feb-2006
Publisher
NATURE PUBLISHING GROUP
Keywords
antigens, CD40; cell differentiation; dendritic cells; killer cells, natural; lipopolysaccharides; Toll-like receptors
Citation
EXPERIMENTAL AND MOLECULAR MEDICINE, v.38, no.2, pp 72 - 84
Pages
13
Journal Title
EXPERIMENTAL AND MOLECULAR MEDICINE
Volume
38
Number
2
Start Page
72
End Page
84
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/15176
DOI
10.1038/emm.2006.9
ISSN
1226-3613
2092-6413
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-alpha, 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 HILA class 11 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 TILR4, a major component of the LPS receptor system, they did not show an enhanced level of CCR7 or cytokine production after ILPS 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, ILPS-stimulated MuDC failed to stimulate primary NK cells. Taken together, our findings suggest that, although MuDC express TLR4, unlike TNF-alpha and IL-1 beta, ILPS does not stimulate MuDC to acquire mature phenotypes, and they may have impaired activity to initiate innate immune response.
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