| First Author | Aguiló JI | Year | 2009 |
| Journal | J Immunol | Volume | 182 |
| Issue | 4 | Pages | 1972-81 |
| PubMed ID | 19201850 | Mgi Jnum | J:144801 |
| Mgi Id | MGI:3831959 | Doi | 10.4049/jimmunol.0801820 |
| Citation | Aguilo JI, et al. (2009) Protein kinase C-theta is required for NK cell activation and in vivo control of tumor progression. J Immunol 182(4):1972-81 |
| abstractText | Protein kinase C-theta (PKCtheta) was initially isolated as an important PKC isoform expressed in T cells, although its expression is not restricted to these cells. Despite the central function of PKCtheta in several immune responses, its role in the antitumor response against MHC class I (MHC-I)-negative cells has not been investigated. This is an important issue because most tumor cells growing in vivo down-regulate MHC-I expression to escape the CTL-mediated response. In the present work, we show that in vivo development of a MHC-I-deficient tumor (RMA-S) is much favored in PKCtheta(-/-) mice compared with wild-type mice. This is associated with a reduced recruitment of NK cells to the site of tumor development and a reduced activation status of recruited NK cells. This correlates with a reduced ex vivo and in vivo cytotoxic potential of NK cells isolated from PKCtheta(-/-) mice treated with polyinosinic:polycytidylic acid. Consistently, polinosinic:cytidilic acid treatment induces PKCtheta expression and activation of its enzymatic activity in NK cells in an indirect manner. These observations underline the relevance of PKCtheta as a key molecule in NK cell-mediated antitumor immune surveillance. |
