The shared epitope (SE) accelerates endogenous reactive oxygen species (ROS) production

<p><b>Copyright information:</b></p><p>Taken from "The rheumatoid arthritis shared epitope increases cellular susceptibility to oxidative stress by antagonizing an adenosine-mediated anti-oxidative pathway"</p><p>http://arthritis-research.com/content/9/1/R5</p><p>Arthritis Research & Therapy 2007;9(1):R5-R5.</p><p>Published online 25 Jan 2007</p><p>PMCID:PMC1865041.</p><p></p> Time-course ROS levels in representative SE-positive (red line) and SE-negative (blue line) B-lymphocyte cell lines. ROS production rates in B lymphocytes. Results are shown as the mean ± standard error of the mean fluorescent units per minute (FU/minute) during the linear late phase of the ROS curve (80 to 200 minutes). Data of the SE-positive (SE+) and SE-negative (SE-) groups were compiled from three to five consecutive experiments in each cell line. The values in parentheses represent the number of donors in each group. ROS levels in M1 cells stimulated with 2.5 μg/ml of either SE-positive hepatitis B core (HBc) capsids (HBc*0401, red line) or SE-negative HBc capsids (HBc*0402, blue line). ROS levels in M1 cells stimulated with 100 μg/ml of either an SE-positive 15 mer peptide (65–79*0401, red circles) or an SE-negative 15 mer peptide (65–79*0402, blue circles). Calculations of values in and were based on paired test analysis. DCF, dichlorofluorescein

The shared epitope (SE) attenuates adenosine-induced protection against oxidative DNA damage

<p><b>Copyright information:</b></p><p>Taken from "The rheumatoid arthritis shared epitope increases cellular susceptibility to oxidative stress by antagonizing an adenosine-mediated anti-oxidative pathway"</p><p>http://arthritis-research.com/content/9/1/R5</p><p>Arthritis Research & Therapy 2007;9(1):R5-R5.</p><p>Published online 25 Jan 2007</p><p>PMCID:PMC1865041.</p><p></p> The potency of adenosine-mediated anti-oxidative signaling was determined in L-cell transfectants expressing cDNA corresponding to (L565.5), (L514.3), or (L259.3). Human M1 fibroblasts were incubated for 1 hour with or without 24 μg/ml of SE-positive (T-DRB1*0401) or SE-negative (T-DRB1*0401) tetrameric molecules. At the end of incubation, the extent of adenosine-induced protection against oxidative DNA damage was determined as above. M1 human fibroblasts were pre-incubated overnight in the absence or presence of 2.5 μg/ml of either HBc*0401 or HBc*0402 multimeric proteins. At the end of incubation, the extent of adenosine-induced protection against oxidative DNA damage was determined. *< 0.05

Additional file 1: Figure S1. of Periodontal bacterial colonization in synovial tissues exacerbates collagen-induced arthritis in B10.RIII mice

Periodontal infection induces active inflammation in polymicrobial infected + CII immunized mice. Polymicrobial-infected + CII immunized mice, left metatarsal tissue H&E staining showing active inflammation with infiltration of neutrophils and macrophages. A × 1 magnification, B × 2 magnification, C × 10 magnification (top panel). I, II, III, IV, and V are digits. CII-immunized mice metatarsal tissue H&E staining showing minimal inflammation (A × 1, B × 2, and C × 10 magnification (bottom panel)). N = 6 in each group. (TIF 2050 kb