Journal
CELL
Volume 179, Issue 5, Pages 1191-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2019.10.028
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Funding
- NCI F32 Ruth L. Kirschstein National Research Service Award individual postdoctoral fellowship (Parent F32) [CA210427]
- NCI Breast SPORE program [P50-CA58223, RO1-CA148761, RO1-CA195740]
- Breast Cancer Research Foundation
- Susan G. Komen [SAC-160074]
- Susan G. Komen Career Catalyst research grant
- Susan G. Komen postdoctoral fellowship [PDF17479425]
- Corsorcio Centro de Investigacion Biomedica en Red, thematic area for cancer (CIBERONC), Instituto de Salud Carlos III, Spain
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This study identifies mechanisms mediating responses to immune checkpoint inhibitors using mouse models of triple-negative breast cancer. By creating new mammary tumor models, we find that tumor mutation burden and specific immune cells are associated with response. Further, we developed a rich resource of single-cell RNA-seq and bulk mRNA-seq data of immunotherapy-treated and non-treated tumors from sensitive and resistant murine models. Using this, we uncover that immune checkpoint therapy induces T follicular helper cell activation of B cells to facilitate the anti-tumor response in these models. We also show that B cell activation of T cells and the generation of antibody are key to immunotherapy response and propose a new biomarker for immune checkpoint therapy. In total, this work presents resources of new preclinical models of breast cancer with large mRNA-seq and single-cell RNA-seq datasets annotated for sensitivity to therapy and uncovers new components of response to immune checkpoint inhibitors.
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