Table III.

Ag reactivity of TIL and persistent T

Patient No.Ag Reactivity of TILaReactivity of Most Prevalent Persistent ClonotypebMost Prevalent Persistent Clonotype (%)
Responder
 6Autol.Autol.16
 9MART-1MART-183
 10MART-1MART-177
 16Autol.Autol.12
 17Autol.Autol.8
 19Autol.N/Tc5
 21Autol.Autol.8
 25Autol.N/T7
 26MART-1-1
 28MART-1MART-17
 30gp100:209–217Autol.7
 31MART-1-2
 34Autol.N/T43
Nonresponder
 7MART-1-<1
 11MART-1-<1
 12Autol.-4
 13MART-1-1
 14Autol.-<1
 15MART-1-4
 18gp100:209–217-<1
 20MART-1-2
 22Autol.-3
 24Autol.N/T17
 27MART-1-1
 29MART-1-<1
  • a Ag reactivity was evaluated by determining the ability of TIL to release IFN-γ in response to autologous (Autol.) or HLA-matched allogeneic tumors, or to T2 cells that were pulsed with either the MART-1:26–35 or gp100:209–217 HLA-A2-restricted peptides.

  • b The Ag reactivity of the most persistent clonotype detected in PBMC 23–63 days after transfer is indicated. Isolated T cell clones corresponding to the dominant persistent clonotypes from TIL from patients 9 and 10 released IFN-γ in response to T2 cells that were pulsed with the MART-1:27–35 peptide, and clones corresponding to the dominant persistent clonotypes within TIL from patients 6, 16, and 22, released IFN-γ in response to autologous tumor cells. The dominant persistent clonotype within the TIL from patient 28 was identified by staining with anti-TRBV Abs and a MART-1:26–35(2L) tetramer. Tumor reactivity of the dominant persistent clonotypes from patients 17 and 30 was determined by measuring the ability of these T cells, which were identified within the TIL using specific TRBV Abs, to specifically up-regulate expression of cell surface CD107a expression following stimulation with autologous tumor cells. A dash indicates either that no persistent clonotype was detected or that the most persistent clonotype was present at a frequency of between 1 and 5% and was not evaluated due to the limited number of cells available for analysis.

  • c For samples designated N/T (not tested), the ability of the persistent clonotype to recognize autologous tumor has not been verified.