@article{06ab0e4e6adb4c34983d100eee97e0aa,
title = "Unleashing Type-2 Dendritic Cells to Drive Protective Antitumor CD4+ T Cell Immunity",
abstract = "A subtype of conventional dendritic cells, cDC2, are able to prime CD4+ T cells for antitumor functions and the presence of cDC2 in human cancer samples may serve as a predictive biomarker for survival and response to immune checkpoint blockade.",
keywords = "CD4 T cells, T cell priming, checkpoint blockade, dendritic cells, immunotherapy, regulatory T cells, tumor immunology, tumor microenvironment",
author = "Mikhail Binnewies and Mujal, {Adriana M.} and Pollack, {Joshua L.} and Combes, {Alexis J.} and Hardison, {Emily A.} and Barry, {Kevin C.} and Jessica Tsui and Ruhland, {Megan K.} and Kelly Kersten and Abushawish, {Marwan A.} and Marko Spasic and Giurintano, {Jonathan P.} and Vincent Chan and Daud, {Adil I.} and Patrick Ha and Ye, {Chun J.} and Roberts, {Edward W.} and Krummel, {Matthew F.}",
note = "Funding Information: We thank E. Wan in the Institute for Human Genetics at UCSF for helping prepare samples for scRNA-seq. We would also like to thank the UCSF Parnassus Flow Cytometry Core for maintenance of flow cytometers and sorters, J.J. Engelhardt and Bristol-Myers-Squibb for Fc-modified anti-CTLA-4 antibodies, S.M. Kaech, M. Conti, and M.D. Rosenblum for mouse strains, L. Rodda for advice related to scRNA-seq, and A. Boissonnas, M.L. Broz, and M.B. Headley for guidance, advice, and critical reading of the manuscript. Acquisition and analysis of certain human samples described in this study was partially funded by contributions from AbbVie , Amgen , Bristol-Myers Squibb , and Pfizer . This work was supported in part by the NSF Graduate Research Fellowship Program awarded to M.B and NIH ( U54 CA163123 , R21CA191428 , and R01 CA197363 ). Funding Information: We thank E. Wan in the Institute for Human Genetics at UCSF for helping prepare samples for scRNA-seq. We would also like to thank the UCSF Parnassus Flow Cytometry Core for maintenance of flow cytometers and sorters, J.J. Engelhardt and Bristol-Myers-Squibb for Fc-modified anti-CTLA-4 antibodies, S.M. Kaech, M. Conti, and M.D. Rosenblum for mouse strains, L. Rodda for advice related to scRNA-seq, and A. Boissonnas, M.L. Broz, and M.B. Headley for guidance, advice, and critical reading of the manuscript. Acquisition and analysis of certain human samples described in this study was partially funded by contributions from AbbVie, Amgen, Bristol-Myers Squibb, and Pfizer. This work was supported in part by the NSF Graduate Research Fellowship Program awarded to M.B and NIH (U54 CA163123, R21CA191428, and R01 CA197363). M.B. A.M.M. and M.F.K. designed experiments. M.B. and A.M.M. performed experiments unless specified. J.L.P. and C.J.Y. participated in the processing and analysis of scRNA-seq. A.C. participated in the design, preparation, and analysis of experiments and acquired and analyzed data related to human samples. E.A.H and J.T. performed tumor growth experiments. K.K. M.K.R. K.C.B. M.A.A. and E.W.R. participated in experimental preparation and analyzing flow cytometry. A.D. M.S. J.P.G. and P.H. facilitated acquisition of human tumor tissue. V.C. managed the acquisition and profiling of human tumors. M.B. A.M.M. and M.F.K. wrote and revised the manuscript. M.B. A.M.M. E.W.R. and M.F.K. edited the manuscript. M.F.K. is a founder, board member, and shareholder in Pionyr Immunotherapeutics that develops novel immunotherapeutics based on tuning of myeloid cells. M.B. J.L.P. and M.A.A. are shareholders in Pionyr Immunotherapeutics. Publisher Copyright: {\textcopyright} 2019 Elsevier Inc.",
year = "2019",
month = apr,
day = "18",
doi = "10.1016/j.cell.2019.02.005",
language = "English (US)",
volume = "177",
pages = "556--571.e16",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "3",
}