The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
Fibrinogen-like Protein 1 Is a Major Immune Inhibitory Ligand of LAG-3
Open accessAbstract
SUMMARY Lymphocyte-activation gene 3 (LAG3) is an immune inhibitory receptor, with major histocompatibility complex class II (MHC-II) as a canonical ligand. However, it remains controversial whether MHC-II is solely responsible for the inhibitory function of LAG3. Here, we demonstrate that fibrinogen-like protein 1 (FGL1), a liver-secreted protein, is a major LAG3 functional ligand independent from MHC-II. FGL1 inhibits antigen-specific T-cell activation and ablation of FGL1 in mice promotes T-cell immunity. Blockade of the FGL1/LAG3 interaction by monoclonal antibodies stimulates tumor immunity and is therapeutic against established mouse tumors in a receptor-ligand inter-dependent manner. FGL1 is highly produced by human cancer cells and elevated FGL1 in the plasma of cancer patients is associated with a poor prognosis and resistance to anti-PD-1/B7-H1 therapy. Our findings reveal an immune evasion mechanism and have implications for the design of cancer immunotherapy.
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Metadata
- Authors
- Wang, J., Sanmamed, M. F., Datar, I., Su, T. T., Ji, L., Sun, J., Chen, L., Chen, Y., Zhu, G., Yin, W., Zheng, L., Zhou, T., Badri, T., Yao, S., Zhu, S., Boto, A., Sznol, M., Melero, I., Vignali, D. A. A., Schalper, K., & Chen, L.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2019-01
- Volume
- 176
- Issue
- 1-2
- Pages
- 334-347.e12
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2906369032
- Cited by
- 871
- References
- 61
- FWCI
- 24.01
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Wang, J., Sanmamed, M. F., Datar, I., Su, T. T., Ji, L., Sun, J., Chen, L., Chen, Y., Zhu, G., Yin, W., Zheng, L., Zhou, T., Badri, T., Yao, S., Zhu, S., Boto, A., Sznol, M., Melero, I., Vignali, D. A. A., . . . Chen, L. (2019). Fibrinogen-like Protein 1 Is a Major Immune Inhibitory Ligand of LAG-3. Cell. https://doi.org/10.1016/j.cell.2018.11.010
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