| First Author | Minguet S | Year | 2008 |
| Journal | Eur J Immunol | Volume | 38 |
| Issue | 9 | Pages | 2475-87 |
| PubMed ID | 18819072 | Mgi Jnum | J:140162 |
| Mgi Id | MGI:3812228 | Doi | 10.1002/eji.200738094 |
| Citation | Minguet S, et al. (2008) Enhanced B-cell activation mediated by TLR4 and BCR crosstalk. Eur J Immunol 38(9):2475-87 |
| abstractText | Despite the important role of B lymphocytes as a bridge between the innate and the adaptive immune system, little is known regarding lipopolysaccharide (LPS) recognition, activation of signalling networks or conceivable cooperation between LPS and the B-cell antigen receptor (BCR). Here, we show that primary B cells can efficiently discriminate between different LPS chemotypes, responding with at least 100-fold higher sensitivity to rough-form LPS compared with smooth-form LPS. Using genetically modified mice, we demonstrate that B lymphocytes recognize all LPS chemotypes via Toll-like receptor 4 (TLR4). In addition, we dissect the signalling pathways that lead to CD69 upregulation upon TLR4 and BCR activation in primary B cells. Our data suggest that TLR4 and BCR induce CD69 transcription via two distinct sets of signalling molecules, exerting quantitative and qualitative differences in B-cell activation. Finally, we show that simultaneous stimulation of TLR4 and BCR additively elevates B-cell activation. In contrast, co-engagement of TLR4 and BCR by antigen-coupled LPS synergistically enhances activation of B cells, pointing out attractive targets for signalling crosstalk in B lymphocytes. |
