Tumor-infiltrating T lymphocytes from renal-cell carcinoma express B7-1 (CD80): T-Cell expansion by T-T cell co-stimulation

✍ Scribed by Martin Thurnher; Christian Radmayr; Alfred Hobisch; Günther Böck; Nikolaus Romani; Georg Bartcch; Helmut Klocker

• Publisher: John Wiley and Sons
• Year: 1995
• Tongue: French
• Weight: 698 KB
• Volume: 62
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910620512

✦ Synopsis

87-I (CD80) provides co-stimulation for T-cell activation by interacting with CD28 or CTLA4. Here we demonstrate the expression of 87-I in freshly isolated and cultured lymphocytes from renal-cell carcinoma. In fresh preparations of lymphocytes infiltrating renal-cell-carcinoma tissue, B7-I mRNA could readily be detected by reverse transcription PCR, and 2-color flowcytometry analysis revealed substantial 87-I expression on T cells from these isolates. As expected, tumor-derived T cells also expressed CD28, the 87 receptor. While B7-I expression of tumor-derived T cells was maintained during culture in interleukin-2-supplemented medium, CD28 expression was further enhanced. We also show that 67-1 is functionally involved in T-cell expansion: anti-B7-I MAb inhibited the PHA-induced proliferation of tumor-derived B7-I + T cells (35s0) in the absence of exogenous antigen-presenting cells, indicating that B7-I mediates T-T cell co-stimulation (self-co-stimulation). Our data demonstrate that T cells infiltrating renal-cell carcinoma express 87-I, and that mutual co-stimulation via the B7-I / CD28 pathway contributes to the interleukin-2-driven expansion of tumor-derived T cells in vitro. The frequency of 87-I + T cells in tumor lesions and the level of 87-1 on these cells may determine the time course of T-cell expansion in vivo. Self-costimulation, however, might also represent one mechanism leading to the state of suppression or anergy characteristic of tumor-infiltrating lymphocytes.