| First Author | Ogata H | Year | 2000 |
| Journal | J Exp Med | Volume | 192 |
| Issue | 1 | Pages | 23-9 |
| PubMed ID | 10880523 | Mgi Jnum | J:63145 |
| Mgi Id | MGI:1860539 | Doi | 10.1084/jem.192.1.23 |
| Citation | Ogata H, et al. (2000) The toll-like receptor protein RP105 regulates lipopolysaccharide signaling in B cells. J Exp Med 192(1):23-9 |
| abstractText | The susceptibility to infections induced by Gram-negative bacteria is largely determined by innate immune responses to bacteria cell wall lipopolysaccharide (LPS). The stimulation of B cells by LPS enhances their antigen-presenting capacity and is accompanied by B cell proliferation and secretion of large quantities of LPS-neutralizing antibodies. Similar to macrophages and neutrophils, the LPS-induced activation of B cells is dependent on Toll-like receptor (TLR)4. Here, we demonstrate that the responses of B cells to LPS are also regulated by another TLR protein, RP105, which is predominantly expressed on mature B cells in mice and humans. The analysis of mice homozygous for the null mutation in the RP105 gene revealed impaired proliferative and humoral immune responses of RP105-deficient B cells to LPS. Using originally LPS-unresponsive Ba/F3 cells expressing exogenous TLR4 and RP105, we demonstrate the functional cooperation between TLR4 and RP105 in LPS-induced nuclear factor kappaB activation. These data suggest the existence of the TLR4-RP105 signaling module in the LPS-induced B cell activation. |
