The present study demonstrates that the transfection of B7-I or its variant MB7-2 genes into MHC class I+ tumor cells (B 16-BL6 or K I 735-M2 melanoma) resulted in the remarkable reduction of lung metastasis caused by i.v. injection into immunocompetent syngeneic mice. However, i.v. injection of the
Heterogeneous effects of B7-1 and B7-2 in the induction of both protective and therapeutic anti-tumor immunity against different mouse tumors
β Scribed by Alfonso Martin-Fontecha; Federica Cavallo; Matteo Bellone; Silvia Heltai; Giandomenica Iezzi; Paola Tornaghi; Nasrin Nabavi; Guido Forni; Paolo Dellabona; Giulia Casorati
- Publisher
- John Wiley and Sons
- Year
- 1996
- Tongue
- English
- Weight
- 911 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
B7-1 (CD80) co-stimulatory molecule gene-transduced Lewis lung carcinoma (LLC) cells (LLC/B7 cells) resulted in remarkable loss of tumorigenicity in syngeneic C57BL/6 mice (87.5% rejection) compared to B7-negative, wild-type LLC (LLC/wt) cells (0% rejection). However, mice that had rejected LLC/B7 c
## Abstract The efficacy of T cellβbased immunotherapy is primarily due to efficient cellular activation that requires the engagement of 2 separate signals, __i.e.__, __via__ the T cell receptor complex and __via__ coβstimulatory molecules the prototype of which is CD28. In cellular activation, the
Although tumor-specific T lymphocytes recognize tumorassociated antigens (TAA) present on their cell surface via major histocompatibility complex (MHC) molecules, T cells require other activating signals. These are provided by costimulatory molecules, including B7-1 (CD80), B7-2 (CD86) and intercell