We considered that this problem could be overcome by the eventual demise

of plasma cells, alone or in combination with B cell depletion. However, plasma cells have very long half-lives, measured in months or even years [11]. Finally, in this study we show that anti-mCD20 mAb depletes B cells efficiently and that, although therapeutically less effective, B cell depletion by this agent is highly efficient for preventing development of experimental Graves’ hyperthyroidism. Our results indicate that B cells are critical not only as antibody-producing cells but also as antigen presenting/immune-modulatory cells in the early phase of the disease pathogenesis. Further studies are necessary to find efficient means to suppress the pathogenic autoantibody production therapeutically as novel therapeutic modalities GSK3235025 ic50 for Graves’ disease and also other autoantibody mediated autoimmune diseases. We thank buy IWR-1 Drs R. Dunn and M. Kehry at Biogen Idec, San Diego, CA, for kind gifts of monoclonal anti-mCD20 (18B12) or control (2B8) antibodies, and Professors Sandra M. McLachlan and Basil Rapoport, at Autoimmune Disease Unit, Cedars-Sinai Medical Center and University of California Los Angeles, CA, for critical reading of the manuscript. The authors have nothing to disclose. “
“Because

Helicobacter pylori has a role in the pathogenesis of gastric cancer, chronic gastritis and peptic ulcer disease, detection of its viable form is very important. The objective of this study

was to optimize a PCR method using ethidium monoazide (EMA) or propidium monoazide (PMA) for selective detection of viable H. pylori cells in mixed samples of viable and dead bacteria. Before conducting the real-time PCR using SodB primers of H. pylori, EMA or PMA was added to suspensions of viable and/or dead H. pylori cells at concentrations between 1 and 100 μM. PMA at a concentration of 50 μM induced the highest DNA loss in dead cells with little loss of genomic DNA in viable cells. In addition, selective detection of viable cells in the oxyclozanide mixtures of viable and dead cells at various ratios was possible with the combined use of PMA and real-time PCR. In contrast, EMA penetrated the membranes of both viable and dead cells and induced degradation of their genomic DNA. The findings of this study suggest that PMA, but not EMA, can be used effectively to differentiate viable H. pylori from its dead form. Helicobacter pylori, a Gram-negative and microaerophilic bacterium that infects human gastrointestinal organs such as the stomach, exhibits various shapes during colonization, including spiral, U-shaped, and coccoid forms (1, 2). H. pylori has a role in the pathogenesis of gastric cancer, chronic gastritis, and peptic ulcer disease (2–5). Social and economic underdevelopment associated with inadequate hygiene practices, consumption of unhealthy food, and paucity of pure drinking water are the main risk factors for the development of H. pylori infection (6).