Scientists have demonstrated that adaptive immunity intervened by T-cell lymphocytes gives important information and support for implementing and maintaining antitumor response. (citation). a broad tumor ingression by cytotoxic CD8+ T cells was heavily correlated with patient survival and react to therapy. Hence, additional studies have observed that cancer reversion and autoimmunity caused by cytotoxic T lymphocyte-associated antigen 4 blockade in patients with metastatic melanoma. Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) is an essential immune-regulatory molecule (showed on triggered T cells and a portion of regulatory T cells) able to down-regulate T cell activation. Blockade of CTLA-4 has been shown in animal models to improve the effectiveness of cancer immunotherapy (citation). This study founded that CTLA-4 is a valuable molecule regulating the resistance to “self” antigens in humans and recommends a role for CTLA-4 blockade in crumbling its tolerance to human cancer antigens for cancer immunotherapy. Furthermore, known that CTLA-4 is not existent on resting T cells but is up regulated for two to three days after T cell activation (citation). Since CTLA-4 seems to impair T cell initiation, efforts have been made to obstruct the antigen-4 activity in murine models of cancer immunotherapy. This analysis was prepared in lab on mice, and the results have exposed that in a transgenic murine model of leading prostate cancer, administrating anti-CTLA-4 plus GM-CSF-expressing prostate cancer cells decreased the development and histological sternness of prostate cancer
Scientists have demonstrated that adaptive immunity intervened by T-cell lymphocytes gives important information and support for implementing and maintaining antitumor response. (citation). a broad tumor ingression by cytotoxic CD8+ T cells was heavily correlated with patient survival and react to therapy. Hence, additional studies have observed that cancer reversion and autoimmunity caused by cytotoxic T lymphocyte-associated antigen 4 blockade in patients with metastatic melanoma. Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) is an essential immune-regulatory molecule (showed on triggered T cells and a portion of regulatory T cells) able to down-regulate T cell activation. Blockade of CTLA-4 has been shown in animal models to improve the effectiveness of cancer immunotherapy (citation). This study founded that CTLA-4 is a valuable molecule regulating the resistance to “self” antigens in humans and recommends a role for CTLA-4 blockade in crumbling its tolerance to human cancer antigens for cancer immunotherapy. Furthermore, known that CTLA-4 is not existent on resting T cells but is up regulated for two to three days after T cell activation (citation). Since CTLA-4 seems to impair T cell initiation, efforts have been made to obstruct the antigen-4 activity in murine models of cancer immunotherapy. This analysis was prepared in lab on mice, and the results have exposed that in a transgenic murine model of leading prostate cancer, administrating anti-CTLA-4 plus GM-CSF-expressing prostate cancer cells decreased the development and histological sternness of prostate cancer