| First Author | Ha YJ | Year | 2004 |
| Journal | J Immunol | Volume | 172 |
| Issue | 1 | Pages | 231-9 |
| PubMed ID | 14688330 | Mgi Jnum | J:87553 |
| Mgi Id | MGI:3027167 | Doi | 10.4049/jimmunol.172.1.231 |
| Citation | Ha YJ, et al. (2004) Role of TNF receptor-associated factor 3 in the CD40 signaling by production of reactive oxygen species through association with p40(phox), a cytosolic subunit of nicotinamide adenine dinucleotide phosphate oxidase. J Immunol 172(1):231-9 |
| abstractText | To extend our previous report, which showed the production of the reactive oxygen species (ROS) after the CD40 ligation in the B cells, we further examined the possible mechanisms for ROS production and the involvement of CD40-induced ROS in p38 activation. Our research shows that the stimulation of WEHI 231 B lymphomas with anti-CD40 induced ROS production and p38 activation. An antioxidant N-acetyl-L-cysteine or an inhibitor for NADPH oxidase blocked both of these, but the inhibitors for 5-lipoxygenase did not. We also show that the treatment of cells with inhibitors for the phosphatidylinositol 3-kinase (PI3-K) interfered with the CD40-induced ROS production and p38 activation. In addition, when overexpressed with a dominant negative form of either Rac1 (N17Rac1) or the TNFR-associated factor (TRAF) 3, the WEHI 231 B cells did not show a full response to the CD40 stimulation to produce ROS. Molecular association studies further revealed that the TRAF3 association with p40(phox), a cytosolic subunit of NADPH oxidase and p85 (a subunit of PI3-K), may possibly be responsible for the production of ROS by CD40 stimulation in WEHI 231 B cells. Collectively, these data suggest that the CD40-induced ROS production by NADPH oxidase in WEHI 231 requires the role of TRAF3, as well as activities of PI3-K and Rac1. |
