TY - JOUR
T1 - Eradication of established tumors by CD8+ T cell adoptive immunotherapy
AU - Hanson, Holly L.
AU - Donermeyer, David L.
AU - Ikeda, Hiroaki
AU - White, J. Michael
AU - Shankaran, Vijay
AU - Old, Lloyd J.
AU - Shiku, Hiroshi
AU - Schreiber, Robert D.
AU - Allen, Paul M.
N1 - Funding Information:
We thank Ching-Yu Huang, Osami Kanagawa, Emil R. Unanue, Kenneth M. Murphy, and Ted H. Hansen for reagents, advice, and valuable discussion. We thank Stephen Horvath, Donna Thompson, and Darren Kreamalmeyer for technical assistance, and we are grateful to Arash Grakoui, Charlie Rice, and Brian Wipke for critical reading of the manuscript. Finally, we thank Jerri Smith for secretarial support in the preparation of this manuscript. This work was supported by National Institutes of Health grant PO1 CA76464. H. L. H. was supported by a predoctoral fellowship from the Howard Hughes Medical Institute.
PY - 2000
Y1 - 2000
N2 - We generated the DUC18 T cell receptor transgenic mouse expressing an H-2K(d) -restricted transgenic T cell receptor specific for the syngeneic CMS5 fibrosarcoma rejection antigen mutated ERK2(136-144). DUC18 mice were capable of specifically eliminating lethal CMS5 tumor challenges, and transfer of DUC18 splenocytes to naive nontransgenic recipients conferred protection from subsequent and established CMS5 tumor burdens. Eradication of established tumor burdens by adoptive transfer of DUC18 splenocytes was dose and time dependent. Transferred tumor-specific T cells remained functional in vivo and capable of rejecting small tumors even in the presence of large, established tumor burdens. These findings highlight the kinetic battle between tumor growth and the production of a tumor-specific response and have critical implications for effective adoptive immunotherapy.
AB - We generated the DUC18 T cell receptor transgenic mouse expressing an H-2K(d) -restricted transgenic T cell receptor specific for the syngeneic CMS5 fibrosarcoma rejection antigen mutated ERK2(136-144). DUC18 mice were capable of specifically eliminating lethal CMS5 tumor challenges, and transfer of DUC18 splenocytes to naive nontransgenic recipients conferred protection from subsequent and established CMS5 tumor burdens. Eradication of established tumor burdens by adoptive transfer of DUC18 splenocytes was dose and time dependent. Transferred tumor-specific T cells remained functional in vivo and capable of rejecting small tumors even in the presence of large, established tumor burdens. These findings highlight the kinetic battle between tumor growth and the production of a tumor-specific response and have critical implications for effective adoptive immunotherapy.
UR - http://www.scopus.com/inward/record.url?scp=0033680870&partnerID=8YFLogxK
U2 - 10.1016/S1074-7613(00)00026-1
DO - 10.1016/S1074-7613(00)00026-1
M3 - Article
C2 - 10981969
AN - SCOPUS:0033680870
SN - 1074-7613
VL - 13
SP - 265
EP - 276
JO - Immunity
JF - Immunity
IS - 2
ER -