Murine B Cell Response to TLR7 Ligands Depends on an IFN-beta Feedback Loop

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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. The Journal of Immunology, 2009, 183: 1569-1576.
Publisher
AMER ASSOC IMMUNOLOGISTS
Issue Date
2009-08
Language
English
Article Type
Article
Keywords

SYSTEMIC-LUPUS-ERYTHEMATOSUS; I INTERFERON RECEPTOR; TOLL-LIKE RECEPTORS; PLASMACYTOID DENDRITIC CELLS; MEDIATED ENHANCEMENT; IMMUNE-COMPLEXES; ALPHA PRODUCTION; MICE; ACTIVATION; DISEASE

Citation

JOURNAL OF IMMUNOLOGY, v.183, no.3, pp.1569 - 1576

ISSN
0022-1767
DOI
10.4049/jimmunol.0803899
URI
http://hdl.handle.net/10203/240848
Appears in Collection
MSE-Journal Papers(저널논문)
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