Lipopolysaccharide can block the potential of monocytes to differentiate into dendritic cells

Citation
Ka. Palucka et al., Lipopolysaccharide can block the potential of monocytes to differentiate into dendritic cells, J LEUK BIOL, 65(2), 1999, pp. 232-240
Citations number
36
Categorie Soggetti
Immunology
Journal title
JOURNAL OF LEUKOCYTE BIOLOGY
ISSN journal
07415400 → ACNP
Volume
65
Issue
2
Year of publication
1999
Pages
232 - 240
Database
ISI
SICI code
0741-5400(199902)65:2<232:LCBTPO>2.0.ZU;2-S
Abstract
We examined whether priming monocytes (MO) with Lipopolysaccharide (LPS) in fluenced their further differentiation into either macrophages (M phi) or d endritic cells (DC), UPS-primed MO differentiated into M phi when cultured further with M phi colony-stimulating factor (M-CSF) but, if cultured then with gramulocyte/M phi (GM)-CSF and IL-4 (interleukin-4), only about 30% of the cells differentiated into CD1a(+)CD14(-) DC and half became CD1a(-)CD1 4(+) M phi. Cytokines present during LPS priming could affect subsequent MO differentiation. Relative to priming with LPS alone, adding M-CSF to LPS d id not modify differentiation of MO to M phi in further culture with RI-CSF , nor did it change the way of differentiation of MO into DC was altered if culture was later switched to GM-CSF/IL-4. Using GM-CSF/IL-4 plus LPS upon priming did not modify differentiation of MO to M phi in further culture w ith M-CSF, as compared to priming with GM-CSF/IL-4 alone, but it counteract ed the effect of LPS on the differentiation of MO to DC in further culture with GM-CSF/IL-4: about 75% of cells then became DC. Alternatively, despite activation by LPS, mature M-CSF-induced M phi preserved the potential to d ifferentiate into DC on subsequent culture with GM-CSF/IL-4. Thus, LPS, a b acterial product known to sustain maturation of MO/M phi as well as of DC, may block the differentiation of MO into DC, except if signal triggering DC differentiation is delivered concomitantly, and modulate in this manner th e induction of adaptive immune responses to infection.