Œ¤‹†”•\‚ðs‚Á‚½Šw‰ïG 20th IUBMB International Congress of Biochemistry and Molecular Biology and 11th FAOBMB Congress.
@@@‚Q‚O‚O‚U”N‚UŒŽ‚P‚W“ú`‚Q‚R“ú (Kyoto)
ƒ^ƒCƒgƒ‹G Increased expression of TLR2 and TLR4 during dimethylsulfoxide-induced neutrophilic differentiation of HL-60 cells
”•\ŽÒGŽñ“¡@„@Ž
@@@iŒF–{‘åŠw@‘åŠw‰@ˆãŠw–òŠwŒ¤‹†•”@ˆâ“`Žq‹@”\‰ž—pŠw•ª–ìj
AbstractG
Neutrophils are the most abundant immune cells found in human blood. These cells possess a wide variety of antimicrobial functions as well as the ability to produce inflammatory cytokines against microorganisms. Recently, it has been shown that human primary neutrophils express most of the toll-like receptors (TLRs), type I transmembrane receptors that play an important role in innate immune recognition of pathogens. However, expression patterns and functions of TLRs during myeloid cell differentiation to neutrophils are unknown. Here, we show that expression of TLR2 and TLR4 genes are strongly up-regulated during dimethylsulfoxide (DMSO)-induced neutrophilic differentiation of HL-60 cells. Moreover, flowcytometry analysis revealed that surface expression of TLR2 and TLR4 were also up-regulated in DMSO-differentiated HL-60 cells (dHL-60 cells). Finally, to determine the function of these receptors in dHL-60 cells, we treated dHL-60 cells with bacterial peptidoglycan (PGN) and lipopolysaccharide (LPS), specific ligands for TLR2 and TLR4, respectively. Real-time quantitative RT-PCR analysis for IL-8 gene showed the hyperresponsiveness to PGN and LPS in dHL-60 cells, but not in undifferentiated HL-60 cells. Thus, these results suggest a differentiation-dependent increase of TLR2 and TLR4 expression, which may be associated with hyperesponsiveness to the bacterial PGN and LPS in dHL-60 cells.
|