Skip to main content
. Author manuscript; available in PMC: 2008 Jan 7.
Published in final edited form as: J Immunol. 2004 Dec 15;173(12):7125–7130. doi: 10.4049/jimmunol.173.12.7125

Table III.

Ag reactivity of TIL and persistent T

Patient No. Ag Reactivity of TILa Reactivity of Most Prevalent Persistent Clonotypeb Most Prevalent Persistent Clonotype (%)
Responder
 6 Autol. Autol. 16
 9 MART-1 MART-1 83
 10 MART-1 MART-1 77
 16 Autol. Autol. 12
 17 Autol. Autol. 8
 19 Autol. N/Tc 5
 21 Autol. Autol. 8
 25 Autol. N/T 7
 26 MART-1 - 1
 28 MART-1 MART-1 7
 30 gp100:209–217 Autol. 7
 31 MART-1 - 2
 34 Autol. N/T 43
Nonresponder
 7 MART-1 - <1
 11 MART-1 - <1
 12 Autol. - 4
 13 MART-1 - 1
 14 Autol. - <1
 15 MART-1 - 4
 18 gp100:209–217 - <1
 20 MART-1 - 2
 22 Autol. - 3
 24 Autol. N/T 17
 27 MART-1 - 1
 29 MART-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.