Murine B Cell Response to TLR7 Ligands Depends on an IFN-β Feedback Loop. Green, N. M., Laws, A., Kiefer, K., Busconi, L., Kim, Y., Brinkmann, M. M., Trail, E. H., Yasuda, K., Christensen, S. R., Shlomchik, M. J., Vogel, S., Connor, J. H., Ploegh, H., Eilat, D., Rifkin, I. R., van Seventer, J. M., & Marshak-Rothstein, A. Journal of immunology (Baltimore, Md. : 1950), 183(3):1569–1576, August, 2009. ![Murine B Cell Response to TLR7 Ligands Depends on an IFN-β Feedback Loop [link]](https://bibbase.org/img/filetypes/link.svg "link")
Paper doi abstract bibtex 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.
@article{green_murine_2009,
title = {Murine {B} {Cell} {Response} to {TLR7} {Ligands} {Depends} on an {IFN}-β {Feedback} {Loop}},
volume = {183},
issn = {0022-1767},
url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929820/},
doi = {10.4049/jimmunol.0803899},
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.},
number = {3},
urldate = {2021-04-15},
journal = {Journal of immunology (Baltimore, Md. : 1950)},
author = {Green, Nathaniel M. and Laws, Amy and Kiefer, Kerstin and Busconi, Liliana and Kim, You-Me and Brinkmann, Melanie M. and Trail, Erin Hodges and Yasuda, Kei and Christensen, Sean R. and Shlomchik, Mark J. and Vogel, Stefanie and Connor, John H. and Ploegh, Hidde and Eilat, Dan and Rifkin, Ian R. and van Seventer, Jean Maguire and Marshak-Rothstein, Ann},
month = aug,
year = {2009},
pmid = {19587008},
pmcid = {PMC2929820},
pages = {1569--1576},
}
Downloads: 0
{"_id":"iNNhxuQaBGpoXenj3","bibbaseid":"green-laws-kiefer-busconi-kim-brinkmann-trail-yasuda-etal-murinebcellresponsetotlr7ligandsdependsonanifnfeedbackloop-2009","author_short":["Green, N. M.","Laws, A.","Kiefer, K.","Busconi, L.","Kim, Y.","Brinkmann, M. M.","Trail, E. H.","Yasuda, K.","Christensen, S. R.","Shlomchik, M. J.","Vogel, S.","Connor, J. H.","Ploegh, H.","Eilat, D.","Rifkin, I. R.","van Seventer, J. M.","Marshak-Rothstein, A."],"bibdata":{"bibtype":"article","type":"article","title":"Murine B Cell Response to TLR7 Ligands Depends on an IFN-β Feedback Loop","volume":"183","issn":"0022-1767","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929820/","doi":"10.4049/jimmunol.0803899","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.","number":"3","urldate":"2021-04-15","journal":"Journal of immunology (Baltimore, Md. : 1950)","author":[{"propositions":[],"lastnames":["Green"],"firstnames":["Nathaniel","M."],"suffixes":[]},{"propositions":[],"lastnames":["Laws"],"firstnames":["Amy"],"suffixes":[]},{"propositions":[],"lastnames":["Kiefer"],"firstnames":["Kerstin"],"suffixes":[]},{"propositions":[],"lastnames":["Busconi"],"firstnames":["Liliana"],"suffixes":[]},{"propositions":[],"lastnames":["Kim"],"firstnames":["You-Me"],"suffixes":[]},{"propositions":[],"lastnames":["Brinkmann"],"firstnames":["Melanie","M."],"suffixes":[]},{"propositions":[],"lastnames":["Trail"],"firstnames":["Erin","Hodges"],"suffixes":[]},{"propositions":[],"lastnames":["Yasuda"],"firstnames":["Kei"],"suffixes":[]},{"propositions":[],"lastnames":["Christensen"],"firstnames":["Sean","R."],"suffixes":[]},{"propositions":[],"lastnames":["Shlomchik"],"firstnames":["Mark","J."],"suffixes":[]},{"propositions":[],"lastnames":["Vogel"],"firstnames":["Stefanie"],"suffixes":[]},{"propositions":[],"lastnames":["Connor"],"firstnames":["John","H."],"suffixes":[]},{"propositions":[],"lastnames":["Ploegh"],"firstnames":["Hidde"],"suffixes":[]},{"propositions":[],"lastnames":["Eilat"],"firstnames":["Dan"],"suffixes":[]},{"propositions":[],"lastnames":["Rifkin"],"firstnames":["Ian","R."],"suffixes":[]},{"propositions":["van"],"lastnames":["Seventer"],"firstnames":["Jean","Maguire"],"suffixes":[]},{"propositions":[],"lastnames":["Marshak-Rothstein"],"firstnames":["Ann"],"suffixes":[]}],"month":"August","year":"2009","pmid":"19587008","pmcid":"PMC2929820","pages":"1569–1576","bibtex":"@article{green_murine_2009,\n\ttitle = {Murine {B} {Cell} {Response} to {TLR7} {Ligands} {Depends} on an {IFN}-β {Feedback} {Loop}},\n\tvolume = {183},\n\tissn = {0022-1767},\n\turl = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929820/},\n\tdoi = {10.4049/jimmunol.0803899},\n\tabstract = {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.},\n\tnumber = {3},\n\turldate = {2021-04-15},\n\tjournal = {Journal of immunology (Baltimore, Md. : 1950)},\n\tauthor = {Green, Nathaniel M. and Laws, Amy and Kiefer, Kerstin and Busconi, Liliana and Kim, You-Me and Brinkmann, Melanie M. and Trail, Erin Hodges and Yasuda, Kei and Christensen, Sean R. and Shlomchik, Mark J. and Vogel, Stefanie and Connor, John H. and Ploegh, Hidde and Eilat, Dan and Rifkin, Ian R. and van Seventer, Jean Maguire and Marshak-Rothstein, Ann},\n\tmonth = aug,\n\tyear = {2009},\n\tpmid = {19587008},\n\tpmcid = {PMC2929820},\n\tpages = {1569--1576},\n}\n\n","author_short":["Green, N. M.","Laws, A.","Kiefer, K.","Busconi, L.","Kim, Y.","Brinkmann, M. M.","Trail, E. H.","Yasuda, K.","Christensen, S. R.","Shlomchik, M. J.","Vogel, S.","Connor, J. H.","Ploegh, H.","Eilat, D.","Rifkin, I. R.","van Seventer, J. M.","Marshak-Rothstein, A."],"key":"green_murine_2009","id":"green_murine_2009","bibbaseid":"green-laws-kiefer-busconi-kim-brinkmann-trail-yasuda-etal-murinebcellresponsetotlr7ligandsdependsonanifnfeedbackloop-2009","role":"author","urls":{"Paper":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929820/"},"metadata":{"authorlinks":{}},"html":""},"bibtype":"article","biburl":"https://bibbase.org/zotero/layaasivakumar","dataSources":["FsBPZHgAjBg95hd5m"],"keywords":[],"search_terms":["murine","cell","response","tlr7","ligands","depends","ifn","feedback","loop","green","laws","kiefer","busconi","kim","brinkmann","trail","yasuda","christensen","shlomchik","vogel","connor","ploegh","eilat","rifkin","van seventer","marshak-rothstein"],"title":"Murine B Cell Response to TLR7 Ligands Depends on an IFN-β Feedback Loop","year":2009}