Perforin dependence of natural killer cell‐mediated tumor control in vivo
- 1 December 1995
- journal article
- research article
- Published by Wiley in European Journal of Immunology
- Vol. 25 (12) , 3514-3516
- https://doi.org/10.1002/eji.1830251246
Abstract
Adaptive immune surveillance by T cells against infections and tumors depends on the presence of antigenic peptides presented by major histocompatibility complex (MHC) molecules. If antigenic tumor‐specific peptides or MHC class I molecules are absent, the adaptive T cell immune response fails. Natural killer (NK) cells seem to complement the specific T cells by recognizing target cells lacking MHC class I (e.g. RMA‐S). The role of perforin, which is crucially involved in T cell and NK cell‐mediated target cell lysis, was evaluated in mice lacking perforin with respect to their capacity to eliminate a syngeneic lymphoid tumor. Here, we show that growth of MHC class I− RMA‐S tumor cells in unprimed mice was controlled by NK cells through perforin‐dependent cytotoxicity.Keywords
This publication has 26 references indexed in Scilit:
- Lymphocyte-mediated Cytotoxicity in vitro and in vivo: Mechanisms and SignificanceImmunological Reviews, 1995
- Two distinct pathways of specific killing revealed by perforin mutant cytotoxic T lymphocytesImmunity, 1994
- Cytotoxicity of fresh NK1.1+ T cell receptor alpha/beta+ thymocytes against a CD4+8+ thymocyte population associated with intact Fas antigen expression on the target.The Journal of Experimental Medicine, 1994
- Fas and Perforin Pathways as Major Mechanisms of T Cell-Mediated CytotoxicityScience, 1994
- Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient miceNature, 1994
- Fas involvement in Ca(2+)-independent T cell-mediated cytotoxicity.The Journal of Experimental Medicine, 1993
- Host resistance directed selectively against H-2-deficient lymphoma variants. Analysis of the mechanism.The Journal of Experimental Medicine, 1985
- Abrogation of metastatic properties of tumour cells by de novo expression of H–2K antigens following H–2 gene transfectionNature, 1985
- Tumorigenicity of cells transformed by adenovirus type 12 by evasion of T-cell immunityNature, 1983
- Expression of class I major histocompatibility antigens switched off by highly oncogenic adenovirus 12 in transformed rat cellsNature, 1983