Murine B Cell Response to TLR7 Ligands Depends on an IFN- Feedback Loop
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Ploegh_Murine b cell.pdf
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Author(s)
Green, Nathaniel M.
Laws, Amy
Kiefer, Kerstin
Busconi, Liliana
Kim, You-Me
Brinkmann, Melanie M.
Trail, Erin Hodges
Yasuda, Kei
Christensen, Sean R.
Shlomchik, Mark J.
Date Issued
July 2009
Journal
Journal of Immunology
Publisher
American Association of Immunologists, Inc.
Citation
Green, N. M., A. Laws, K. Kiefer, L. Busconi, Y.-M. Kim, M. M. Brinkmann, E. H. Trail, et al. “Murine B Cell Response to TLR7 Ligands Depends on an IFN- Feedback Loop.” The Journal of Immunology 183, no. 3 (July 20, 2009): 1569-1576.
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Author's final manuscript
Abstract
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-β 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.
MIT Department
Massachusetts Institute of Technology. Department of Biology
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DOI of Published Version
https://doi.org/10.4049/jimmunol.0803899
