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Induction of Tolerance by Porphyromonas gingivalis on APCs: a Mechanism Implicated in Periodontal Infection

N. Cohen1,*,2, J. Morisset2, and D. Emilie1

1 INSERM U131, Institut Paris-Sud sur les Cytokines, 32 rue des Carnets, 92140 Clamart, France; and
2 Department of Oral Biology, Faculty of Dental Medicine, 5 rue Garancière 75006 Paris, France;



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Figure 1. Surface expression of TLR-2 on THP-1 (A), dendritic cells (B), and monocytes (C). Cells were incubated in medium alone or stimulated with E. coli (Ec) or P. gingivalis (Pg) LPS for 24 hrs. Cells were either left untreated ({blacksquare}) or pre-incubated with IL-10 () or Dex ({square}) 24 hrs before stimulation. The level of TLR2 expression was determined by flow cytometry. Data are expressed as % of positive cells ± SD (n = 4). *p < 0.05.

 


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Figure 2. CCL5 and CCL3 production by THP-1. (A) Cells were incubated in medium alone or stimulated with E. coli (Ec) or P. gingivalis (Pg) LPS for 24 hrs. Cells were either left untreated or pre-incubated with IL-10 or Dex 24 hrs before stimulation. (B) Cells were incubated with or without E. coli (Ec) or P. gingivalis (Pg) LPS (Primary stimulation) and then restimulated or not 24 hrs later with Ec.LPS or Pg.LPS (Secondary stimulation). Cell-free supernatants were analyzed by ELISA for CCL3 ({square}) and CCL5 ({blacksquare}) concentration. Data are expressed as means ± SD (n = 3). *p < 0.05.

 


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Figure 3. Surface expression of ILT-3 and B7-H1 on monocytes. Monocytes were incubated in medium alone or stimulated with Pg.LPS or Ec.LPS for 24 hrs and then re-stimulated or not 24 hrs later with Ec.LPS ({square}) or Pg.LPS ({blacksquare}). The levels of B7-H1 ({square}) and ILT-3 ({blacksquare}) were determined by flow cytometry. Data are expressed as the mean fluorescence intensity (MFI) ± SD (n = 4).

 





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Journal of Dental Research ® Critical Reviews (1990-2004)
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