Human papillomavirus type 16 nucleoprotein E7 is a tumor rejection antigen.
AUTOR(ES)
Chen, L P
RESUMO
It has been speculated that immunological mechanisms play an important role in the control of carcinomas associated with human papillomavirus (HPV), such as cervical cancers. We have now demonstrated that immunization of C3H/HeN mice by syngeneic nontumorigenic fibroblast-like cells that contain the transfected HPV-16 E7 gene conferred protection against transplanted cells from a HPV-16 E7-positive syngeneic tumor. This protection was HPV-16 E7-specific and was mediated by CD8+ lymphocytes, which presumably were cytotoxic T lymphocytes. These results indicate that tumor cells containing HPV-16 E7, either as a result of transfection, as in our studies, or naturally, as occurs in many human carcinomas, can induce a tumor-specific rejection response and serve as targets for such a response. The system described here provides an animal model to further study immune responses to HPV-associated malignancies and to test the efficacy of anti-HPV vaccines toward the therapy and prevention of such tumors.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=50759Documentos Relacionados
- Mutational analysis of human papillomavirus type 16 E7 functions.
- A point mutational analysis of human papillomavirus type 16 E7 protein.
- Human Papillomavirus Type 16 E7 Oncoprotein Represses Transcription of Human Fibronectin
- Degradation of the Retinoblastoma Tumor Suppressor by the Human Papillomavirus Type 16 E7 Oncoprotein Is Important for Functional Inactivation and Is Separable from Proteasomal Degradation of E7
- The E7 gene of human papillomavirus type 16 is sufficient for immortalization of human epithelial cells.