Figure 5.
Regulation and function of CCR9. (a) Up-regulation of CCR9 on THP-1 monocytic cells by TNFα. Cells were cultured for 16
hours in the absence or presence of various concentrations of TNFα, then analysed
for CCR9 expression by flow cytometry, *P < 0.05 and **P < 0.01 compared to the absence of TNFα. (b) Chemotactic response of peripheral blood monocytes from healthy donors to increasing
concentrations of CCL25, CCL2 (MCP-1) as positive control, from 1 representative healthy
donor in duplicate.** = P < 0.01 compared to control. (c, d) CCL25 stimulates CD36 expression by RA (c) and non-RA (d) monocytes. Peripheral blood
monocytes were isolated and treated with CCL25, CXCL16 or PMA for three hours, followed
by flow cytometry to detect CD36. Data for CCL25 and PMA are means ± standard errors
from five RA and non-RA individuals all in triplicate. *** = P < 0.0001 compared to control (no CCL25). The rise in CD36 expression in response to
CCL25 is greater for RA (c) than healthy (d) monocytes (P < 0.01 at 50 ng/ml, P < 0.001 at 100 ng/ml and 500 ng/ml CCL25 compared to control). The CXCL16 data represent
two RA and two non-RA individuals in triplicate.
Schmutz et al. Arthritis Research & Therapy 2010 12:R161 doi:10.1186/ar3120 |