The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
CTLA-4: a negative regulator of autoimmune disease.
Open accessAbstract
CTLA-4, a CD28 homologue expressed on activated T cells, binds with high affinity to the CD28 ligands, B7-1 (CD80) and B7-2 (CD86). This study was designed to examine the role of CTLA-4 in regulating autoimmune disease. Murine relapsing-remitting experimental autoimmune encephalomyelitis (R-EAE) is a demyelinating disease mediated by PLP139-151-specific CD4+ T cells in SJL/J mice. Anti-CTLA-4 mAbs (or their F(ab) fragments) enhanced in vitro proliferation and pro-inflammatory cytokine production by PLP139-151-primed lymph node cells. Addition of either reagent to in vitro activation cultures potentiated the ability of T cells to adoptively transfer disease to naive recipients. In vivo administration of anti-CTLA-4 mAb to recipients of PLP139-151-specific T cells resulted in accelerated and exacerbated disease. Finally, anti-CTLA-4 treatment of mice during disease remission resulted in the exacerbation of relapses. Collectively, these results suggest that CTLA-4 mediates the downregulation of ongoing immune responses and plays a major role in regulating autoimmunity.
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Citations
Cites
Lymphoproliferative Disorders with Early Lethality in Mice Deficient in Ctla-4
Waterhouse, P., Penninger, J. M., Timms, E., Wakeham, A., Shahinian, A., Lee, K. P., Thompson, C. B., Griesser, H., & Mak, T. W. (1995) · Science · doi:10.1126/science.270.5238.985 · Cited by 2,766
CD28 and CTLA-4 have opposing effects on the response of T cells to stimulation.
Krummel, M. F., & Allison, J. P. (1995) · The Journal of experimental medicine · doi:10.1084/jem.182.2.459 · Cited by 2,245 · cited 1×
“Cross-linking of CTLA-4 after the ligation of CD3 and CD28 strongly inhibited proliferation and IL-2 production (14).”
BackgroundCTLA-4 is a second receptor for the B cell activation antigen B7.
Linsley, P. S., Brady, W., Urnes, M., Grosmaire, L. S., Damle, N. K., & Ledbetter, J. A. (1991) · The Journal of experimental medicine · doi:10.1084/jem.174.3.561 · Cited by 1,685
Cited by
Takahashi, T., Tagami, T., Yamazaki, S., Uede, T., Shimizu, J., Sakaguchi, N., Mak, T. W., & Sakaguchi, S. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.192.2.303 · Cited by 2,233
Salomon, B., Lenschow, D. J., Rhee, L., Ashourian, N., Singh, B., Sharpe, A., & Bluestone, J. A. (2000) · Immunity · doi:10.1016/s1074-7613(00)80195-8 · Cited by 2,081
Self-citationAnti–PD-1/PD-L1 therapy of human cancer: past, present, and future
Chen, L., & Han, X. (2015) · Journal of Clinical Investigation · doi:10.1172/jci80011 · Cited by 1,437
CTLA-4–Ig regulates tryptophan catabolism in vivo
Grohmann, U., Orabona, C., Fallarino, F., Vacca, C., Calcinaro, F., Falorni, A., Candeloro, P., Belladonna, M. L., Bianchi, R., Fioretti, M. C., et al. (2002) · Nature Immunology · doi:10.1038/ni846 · Cited by 1,161
CTLA-4: new insights into its biological function and use in tumor immunotherapy
Egen, J. G., Kuhns, M. S., & Allison, J. P. (2002) · Nature Immunology · doi:10.1038/ni0702-611 · Cited by 940
Metadata
- Authors
- Karandikar, N. J., Vanderlugt, C. L., Walunas, T. L., Miller, S. D., & Bluestone, J. A.
- Venue
- The Journal of experimental medicine
- Publisher
- Rockefeller University Press
- Published
- 1996-08-01
- Volume
- 184
- Issue
- 2
- Pages
- 783-788
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2114329158
- Cited by
- 376
- References
- 3
- FWCI
- 11.01
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Karandikar, N. J., Vanderlugt, C. L., Walunas, T. L., Miller, S. D., & Bluestone, J. A. (1996). CTLA-4: a negative regulator of autoimmune disease. The Journal of experimental medicine. https://doi.org/10.1084/jem.184.2.783
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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.
