| First Author | Green NM | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 3 | Pages | 1569-76 |
| PubMed ID | 19587008 | Mgi Jnum | J:151708 |
| Mgi Id | MGI:4355097 | Doi | 10.4049/jimmunol.0803899 |
| Citation | Green NM, et al. (2009) Murine B cell response to TLR7 ligands depends on an IFN-beta feedback loop. J Immunol 183(3):1569-76 |
| abstractText | Type I IFNs play an important, yet poorly characterized, role in systemic lupus erythematosus. To better understand the interplay between type I IFNs and the activation of autoreactive B cells, we evaluated the effect of type I IFN receptor (IFNAR) deficiency in murine B cell responses to common TLR ligands. In comparison to wild-type B cells, TLR7-stimulated IFNAR(-/-) B cells proliferated significantly less well and did not up-regulate costimulatory molecules. By contrast, IFNAR1(-/-) B cells did not produce cytokines, but did proliferate and up-regulate activation markers in response to other TLR ligands. These defects were not due to a difference in the distribution of B cell populations or a failure to produce a soluble factor other than a type I IFN. Instead, the compromised response pattern reflected the disruption of an IFN-beta feedback loop and constitutively low expression of TLR7 in the IFNAR1(-/-) B cells. These results highlight subtle differences in the IFN dependence of TLR7 responses compared with other TLR-mediated B cell responses. |
