The DOI matches its Crossref record; 26 of the 26 references it cites were found in a registry or an index.
Loss of the lupus autoantigen Ro52/Trim21 induces tissue inflammation and systemic autoimmunity by disregulating the IL-23–Th17 pathway
Open accessAbstract
Ro52/Trim21 is targeted as an autoantigen in systemic lupus erythematosus and Sjögren's syndrome. Polymorphisms in the Ro52 gene have been linked to these autoimmune conditions, but the molecular mechanism by which Ro52 may promote development of systemic autoimmune diseases has not been explored. To address this issue, we generated Ro52-null mice (Ro52−/−), which appear phenotypically normal if left unmanipulated. However, Ro52−/− mice develop severe dermatitis extending from the site of tissue injury induced by ear tags. The affected mice further develop several signs of systemic lupus with hypergammaglobulinemia, autoantibodies to DNA, proteinuria, and kidney pathology. Ro52, which was recently identified as an E3 ligase, mediates ubiquitination of several members of the interferon regulatory factor (IRF) family, and the Ro52-deficient mice have an enhanced production of proinflammatory cytokines that are regulated by the IRF transcription factors, including cytokines involved in the Th17 pathway (interleukin [IL] 6, IL-12/IL-23p40, and IL-17). Loss of IL-23/IL-17 by genetic deletion of IL-23/p19 in the Ro52−/− mice conferred protection from skin disease and systemic autoimmunity. These data reveal that the lupus-associated Ro52 protein is an important negative regulator of proinflammatory cytokine production, and they provide a mechanism by which a defective Ro52 function can lead to tissue inflammation and systemic autoimmunity through the IL-23–Th17 pathway.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Bettelli, E., Carrier, Y., Gao, W., Korn, T., Strom, T. B., Oukka, M., Weiner, H. L., & Kuchroo, V. K. (2006) · Nature · doi:10.1038/nature04753 · Cited by 6,992
Self-citationCua, D. J., Sherlock, J., Chen, Y., Murphy, C. A., Joyce, B., Seymour, B., Lucian, L., To, W., Kwan, S., Churakova, T., et al. (2003) · Nature · doi:10.1038/nature01355 · Cited by 2,906
The tripartite motif family identifies cell compartments
Reymond, A., Meroni, G., Fantozzi, A., Merla, G., Cairo, S., Luzi, L., Riganelli, D., Zanaria, E., Messali, S., Cainarca, S., et al. (2001) · The EMBO Journal · doi:10.1093/emboj/20.9.2140 · Cited by 1,366
Crispín, J. C., Oukka, M., Bayliss, G., Cohen, R. A., Van Beek, C. A., Stillman, I. E., Kyttaris, V. C., Juang, Y.-T., & Tsokos, G. C. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.181.12.8761 · Cited by 789
Graham, R. R., Kozyrev, S. V., Baechler, E. C., Reddy, M. V. P. L., Plenge, R. M., Bauer, J. W., Ortmann, W. A., Koeuth, T., Escribano, M. F. G., Collaborative Groups, T. A. A. S., et al. (2006) · Nature Genetics · doi:10.1038/ng1782 · Cited by 671
Sigurdsson, S., Nordmark, G., Göring, H. H. H., Lindroos, K., Wiman, A.-C., Sturfelt, G., Jönsen, A., Rantapää-Dahlqvist, S., Möller, B., Kere, J., et al. (2005) · The American Journal of Human Genetics · doi:10.1086/428480 · Cited by 607
Self-citationWong, C. K., Lit, L. C. W., Tam, L. S., Li, E. K. M., Wong, P. T. Y., & Lam, C. W. K. (2008) · Clinical Immunology · doi:10.1016/j.clim.2008.01.019 · Cited by 532
The type I interferon system in systemic lupus erythematosus
Rönnblom, L., Eloranta, M., & Alm, G. V. (2006) · Arthritis & Rheumatism · doi:10.1002/art.21571 · Cited by 341
Self-citationHiggs, R., Gabhann, J. N., Larbi, N. B., Breen, E. P., Fitzgerald, K. A., & Jefferies, C. A. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.181.3.1780 · Cited by 310
Self-citationNguyen, C. Q., Hu, M. H., Li, Y., Stewart, C., & Peck, A. B. (2008) · Arthritis & Rheumatism · doi:10.1002/art.23214 · Cited by 290
Cited by
Mouse and human FcR effector functions
Bruhns, P., & Jönsson, F. (2015) · Immunological Reviews · doi:10.1111/imr.12350 · Cited by 579
Regulating IRFs in IFN Driven Disease
Jefferies, C. A. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00325 · Cited by 365
Self-citationTRIMmunity: The Roles of the TRIM E3-Ubiquitin Ligase Family in Innate Antiviral Immunity
Rajsbaum, R., García-Sastre, A., & Versteeg, G. A. (2014) · Journal of Molecular Biology · doi:10.1016/j.jmb.2013.12.005 · Cited by 353
Epithelial–immune cell interplay in primary Sjögren syndrome salivary gland pathogenesis
Verstappen, G. M., Pringle, S., Bootsma, H., & Kroese, F. G. M. (2021) · Nature Reviews Rheumatology · doi:10.1038/s41584-021-00605-2 · Cited by 298
TRIM21 Ubiquitylates SQSTM1/p62 and Suppresses Protein Sequestration to Regulate Redox Homeostasis
Pan, J.-A., Sun, Y., Jiang, Y.-P., Bott, A. J., Jaber, N., Dou, Z., Yang, B., Chen, J.-S., Catanzaro, J. M., Du, C., et al. (2016) · Molecular Cell · doi:10.1016/j.molcel.2016.02.007 · Cited by 265
Metadata
- Authors
- Espinosa, A., Dardalhon, V., Brauner, S., Ambrosi, A., Higgs, R., Quintana, F. J., Sjöstrand, M., Eloranta, M.-L., Ní Gabhann, J., Winqvist, O., Sundelin, B., Jefferies, C. A., Rozell, B., Kuchroo, V. K., & Wahren-Herlenius, M.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2009-07-27
- Volume
- 206
- Issue
- 8
- Pages
- 1661-1671
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2122543047
- Cited by
- 313
- References
- 26
- FWCI
- 18.81
- Type
- journal article
- Language
- en
- Open access
- bronze
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Loss of the lupus autoantigen Ro52/Trim21 induces tissue inflammation and systemic autoimmunity by disregulating the IL-23–Th17 pathway. https://app.cochat.ai/papers/10.1084/jem.20090585
- The paper
- Espinosa, A., Dardalhon, V., Brauner, S., Ambrosi, A., Higgs, R., Quintana, F. J., Sjöstrand, M., Eloranta, M.-L., Ní Gabhann, J., Winqvist, O., Sundelin, B., Jefferies, C. A., Rozell, B., Kuchroo, V. K., & Wahren-Herlenius, M. (2009). Loss of the lupus autoantigen Ro52/Trim21 induces tissue inflammation and systemic autoimmunity by disregulating the IL-23–Th17 pathway. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20090585
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
