TIM-3 on myeloid cells promotes pulmonary inflammation through increased production of galectin-3
Author:
Funder
National Cancer Center
National Research Foundation of Korea
Publisher
Springer Science and Business Media LLC
Link
https://www.nature.com/articles/s42003-024-06762-w.pdf
Reference70 articles.
1. Monney, L. et al. Th1-specific cell surface protein Tim-3 regulates macrophage activation and severity of an autoimmune disease. Nature 415, 536–541 (2002).
2. Anderson, A. C. et al. Promotion of tissue inflammation by the immune receptor Tim-3 expressed on innate immune cells. Science 318, 1141–1143 (2007).
3. Chiba, S. et al. Tumor-infiltrating DCs suppress nucleic acid-mediated innate immune responses through interactions between the receptor TIM-3 and the alarmin HMGB1. Nat. Immunol. 13, 832–842 (2012).
4. Gleason, M. K. et al. Tim-3 is an inducible human natural killer cell receptor that enhances interferon gamma production in response to galectin-9. Blood 119, 3064–3072 (2012).
5. Nebbia, G. et al. Upregulation of the Tim-3/galectin-9 pathway of T cell exhaustion in chronic hepatitis B virus infection. PLoS One 7, e47648 (2012).
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