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27-Hydroxycholesterol (27OHChol) also rapidly induces the differentiation of THP1 cells into mDCs [14] with high expression of mDC-specific markers such as CD80, CD83, CD86, and CD88.
After incubation with Dx and 27OHChol, THP-1 cells were harvested and incubated for 2h at 4[degrees]C with antibodies against CD80, CD83, CD88, CD105, CD137, CD166, and major histocompatibility complex (MHC) class I and II molecules, followed by washing and incubation with fluorescent dye-conjugated secondary antibodies.
The levels of CD80, CD83, and CD88 were increased 4.
The percentages of control cells positive for CD80, CD83, and CD88 were 8.
It is possible that downregulated expression of CD80, CD83, and CD88 by Dx can affect pathogenesis of atherosclerosis.
2, TfR, CD166, CD44, CD88, and CD98, indicating that it plays a significant role in immune suppression [6, 15, 30, 31, 37, 46, 95, 96].
Interestingly, while toddaculin at 250 [micro]M was able to induce apoptosis in U-937 cells, involving decreased phosphorytation levels of ERIC and Akt, 50 [micro]M toddaculin exerted differentiating effects, inducing both the capacity of U-937 cells to reduce NBT and the expression of differentiation markers CD88 and CD11 b, but no change in p-Akt or p-ERK levels.
In this regard, at higher concentrations toddaculin (6) induced U-937 cell death mediated by caspase cascade activation and down-regulation of ERK 1/2 and serine/threonine protein kinase Akt phosphorylation, whereas at lower concentrations it induced NBT reduction and expression of CD1lb and CD88 monocytic differentiation markers.
Determination of CD88 expression, NBT reduction capacity and chernotactic response
6A, D and E shows the inducing effect of a 48-11 treatment with 50 [micro]M toddaculin (6) on CD11b) expression, NBT reduction capacity and functional CD88 expression in U-937 cells, respectively.