The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Targeted Deletion of fgl2 Leads to Impaired Regulatory T Cell Activity and Development of Autoimmune Glomerulonephritis
Open accessAbstract
Mice with targeted deletion of fibrinogen-like protein 2 (fgl2) spontaneously developed autoimmune glomerulonephritis with increasing age, as did wild-type recipients reconstituted with fgl2−/− bone marrow. These data implicate FGL2 as an important immunoregulatory molecule and led us to identify the underlying mechanisms. Deficiency of FGL2, produced by CD4+CD25+ regulatory T cells (Treg), resulted in increased T cell proliferation to lectins and alloantigens, Th 1 polarization, and increased numbers of Ab-producing B cells following immunization with T-independent Ags. Dendritic cells were more abundant in fgl2−/− mice and had increased expression of CD80 and MHCII following LPS stimulation. Treg cells were also more abundant in fgl2−/− mice, but their suppressive activity was significantly impaired. Ab to FGL2 completely inhibited Treg cell activity in vitro. FGL2 inhibited dendritic cell maturation and induced apoptosis of B cells through binding to the low-affinity FcγRIIB receptor. Collectively, these data suggest that FGL2 contributes to Treg cell activity and inhibits the development of autoimmune disease.
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
Sakaguchi, S. (2005) · Nature Immunology · doi:10.1038/ni1178 · Cited by 2,669
A function for interleukin 2 in Foxp3-expressing regulatory T cells
Fontenot, J. D., Rasmussen, J. P., Gavin, M. A., & Rudensky, A. Y. (2005) · Nature Immunology · doi:10.1038/ni1263 · Cited by 1,819
Genome-wide analysis of Foxp3 target genes in developing and mature regulatory T cells
Zheng, Y., Josefowicz, S. Z., Kas, A., Chu, T.-T., Gavin, M. A., & Rudensky, A. Y. (2007) · Nature · doi:10.1038/nature05563 · Cited by 835
Cited by
Mechanisms of Foxp3+ T Regulatory Cell-Mediated Suppression
Shevach, E. M. (2009) · Immunity · doi:10.1016/j.immuni.2009.04.010 · Cited by 1,754
Joller, N., Lozano, E., Burkett, P. R., Patel, B., Xiao, S., Zhu, C., Xia, J., Tan, T. G., Sefik, E., Yajnik, V., et al. (2014) · Immunity · doi:10.1016/j.immuni.2014.02.012 · Cited by 955
Mitochondrial complex III is essential for suppressive function of regulatory T cells
Weinberg, S. E., Singer, B. D., Steinert, E. M., Martinez, C. A., Mehta, M. M., Martínez-Reyes, I., Gao, P., Helmin, K. A., Abdala-Valencia, H., Sena, L. A., et al. (2019) · Nature · doi:10.1038/s41586-018-0846-z · Cited by 494
Regulatory T cells generated early in life play a distinct role in maintaining self-tolerance
Yang, S., Fujikado, N., Kolodin, D., Benoist, C., & Mathis, D. (2015) · Science · doi:10.1126/science.aaa7017 · Cited by 443
Dwyer, D. F., Ordovas-Montanes, J., Allon, S. J., Buchheit, K. M., Vukovic, M., Derakhshan, T., Feng, C., Lai, J., Hughes, T. K., Nyquist, S. K., et al. (2021) · Science Immunology · doi:10.1126/sciimmunol.abb7221 · Cited by 175
Metadata
- Authors
- Shalev, I., Liu, H., Koscik, C., Bartczak, A., Javadi, M., Wong, K. M., Maknojia, A., He, W., Liu, M. F., Diao, J., Winter, E., Manuel, J., McCarthy, D., Cattral, M., Gommerman, J., Clark, D. A., Phillips, M. J., Gorczynski, R. R., Zhang, L., Downey, G., Grant, D., Cybulsky, M. I., & Levy, G.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-01-01
- Volume
- 180
- Issue
- 1
- Pages
- 249-260
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1934905808
- Cited by
- 160
- References
- 3
- FWCI
- 3.15
- 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: Targeted Deletion of fgl2 Leads to Impaired Regulatory T Cell Activity and Development of Autoimmune Glomerulonephritis. https://app.cochat.ai/papers/10.4049/jimmunol.180.1.249
- The paper
- Shalev, I., Liu, H., Koscik, C., Bartczak, A., Javadi, M., Wong, K. M., Maknojia, A., He, W., Liu, M. F., Diao, J., Winter, E., Manuel, J., McCarthy, D., Cattral, M., Gommerman, J., Clark, D. A., Phillips, M. J., Gorczynski, R. R., Zhang, L., . . . Levy, G. (2008). Targeted Deletion of fgl2 Leads to Impaired Regulatory T Cell Activity and Development of Autoimmune Glomerulonephritis. The Journal of Immunology. https://doi.org/10.4049/jimmunol.180.1.249
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.
