Interleukin 7 enhances the proliferation and effector function of tumor-infiltrating lymphocytes from renal-cell carcinoma

✍ Scribed by Dante Sica; Patricia Rayman; Jill Stanley; James H. Finke; Eric Klein; Eric Klein; Mark Edinger; Raymond R. Tubbs; Ronald Bukowski

• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: French
• Weight: 794 KB
• Volume: 53
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910530613

✦ Synopsis

Previous studies have documented the effects of 112 on the growth and effector function of tumor-infiltrating lymphocytes (TlL) in cancer patients. Since IL7 is known to induce Tand NK-cell responses in the peripheral blood, we examined the immuno-enhancing effects of 117 on TIL derived from human renal-cell carcinoma (RCC). Whereas I12 induced the growth of freshly isolated TIL in vitro, IL7 was ineffective alone and failed to increase the total number of cells proliferating to 112. However, 117 did provide a proliferative signal to TIL that were initially expanded in culture with either 1L2 or 112/IL7 for 2 weeks. IL7 also induced the proliferation of CD4+ and CD8+ TIL lines that have specificity for RCC. The proliferative response induced by IL7 was independent of In. since anti-112 antibodies did not block 117-induced proliferation of TIL. 117 did cooperate with anti-CD3 stimulation for the induction of proliferation; however, the magnitude of this interaction was variable and the response usually additive. In addition, 117 synergized with anti-CD3 to induce the secretion of IFNy from short-tenncultured TIL and from a TIL line. Although 117 did not promote the development of a tumor-specific T-cell response from 112-expanded TIL, tL7 enhanced lymphokine-activated killer (LAK) activity from some short-term-cultured 111. These results illustrate that 117 can potentiate the growth and production of IFNy from RCC-reactive TIL and, to a lesser extent, enhance 112-induced I A K activity of TIL.