Skip to main content
. 2005 Dec;7(12):1112–1122. doi: 10.1593/neo.05442

Table 1.

Response to Proinflammatory and Pathogen-Derived Factors.

CC LPS Poly I:C CpG ODN

DC DR+IC DC DR+IC DC DR+IC DC DR+IC
CD40 351.9 ± 52.3** 82.4 ± 8.7** 344.4 ± 45.6** 122.0 ± 12.9** 175.6 ± 76.5** 57.9 ± 28.4** 218.3 ± 21.5 93.9 ± 33.3
CD80 17.3 ± 4.6** 0.6 ± 1.4** 34.7 ± 8.3** 4.4 ± 1.5** 22.6 ± 6.6** 3.5 ± 0.8** 10.0 ± 1.7 3.7 ± 3.3
CD83 65.2 ± 12.9** 9.14 ± 2.8** 40.9 ± 5.0*** 10.0 ± 2.3*** 20.3 ± 9.2** 6.4 ± 1.9** 77.9 ± 13.2* 24.3 ± 16.1*
CD86 729.51 ± 100.*** 314.5 ± 6.3*** 703.6 ± 85.6*** 22.9 ± 10.6*** 348.7 ± 159.5* 21.8 ± 5.3* 477.2 ± 32.9*** 3.6 ± 1.6***
HLA-DR 1046.5 ± 20.6* 273.9 ± 47.3* 1044.1 ± 56.7* 168.9 ± 60.7* 458.0 ± 70.8** 135.8 ± 29.0** 663.6 ± 209.5 297.5 ± 120.7

Phenotypic maturation of DC and DR+IC was analyzed in PBMC following incubation with a combination of proinflammatory cytokines (TNF-α, IL-1β, IL-6, and PGE2; CC) or pathogen-derived factors, including ligands for TLR4 (LPS), TLR3 (poly I:C), and TLR9 (CpG ODN). Data were collected from 16 patients with breast cancer (stage II, n = 9; stage IV, n = 7). The magnitude of the response is expressed as ΔMFI (MFI of stimulated cells - MFI of unstimulated cells) ± SEM. Statistically significant differences between DC and DR+IC are indicated.

*

P < .05.

**

P < .01.

***

P < .001.

HHS Vulnerability Disclosure