期刊
CANCER CELL
卷 37, 期 5, 页码 674-+出版社
CELL PRESS
DOI: 10.1016/j.ccell.2020.03.016
关键词
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资金
- ISREC Foundation
- SNF
- SCL
- Emma Muschamp Foundation
- Fondation Aclon
- Clinician Scientist Program of the Medical Faculty, Ulm University
Genomic alterations in cancer cells can influence the immune system to favor tumor growth. In non-Hodgkin lymphoma, physiological interactions between B cells and the germinal center microenvironment are coopted to sustain cancer cell proliferation. We found that follicular lymphoma patients harbor a recurrent hotspot mutation targeting tyrosine 132 (Y132D) in cathepsin S (CTSS) that enhances protein activity. CTSS regulates antigen processing and CD4(+) and CD8(+) T cell-mediated immune responses. Loss of CTSS activity reduces lymphoma growth by limiting communication with CD4(+) T follicular helper cells while inducing antigen diversification and activation of CD8(+) T cells. Overall, our results suggest that CTSS inhibition has non-redundant therapeutic potential to enhance anti-tumor immune responses in indolent and aggressive lymphomas.
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