Immune Regulation Inhibition and Its Usage and Effectiveness In Cancer Therapy
The existence of inhibitory pathways that limit T-cell response has been the target of checkpoint inhibitors, the best example is CTLA-4 which inhibits T-cell activity by binding to B7 and interfering with CD28-B7 costimulation and by binding to CD-80 and CD-86 (1) in addition to programmed cell death (PD-1) first discovered in mice, carries a role in inducing "peripheral tolerance" of T cells by binding to PDL-1 in APCs and thereby stopping an immune response(2) the mechanism of PD-1 blockade, which is induced by IFN-y
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Different cancers affect millions of people around the world and is considered one of humanity's greatest challenges, traditionally cancer is tackled by therapeutic methods such as radiation or surgery, chemotherapy as well as transplant. Activating immune cells is a relatively old concept dating back to the early 20th century, whereby they would be able to attack cancer cells via CD8 T cytotoxic cells but the inherent principle of our immune system is the ability to distinguish "self" from "non-self", for example when the T cells recognize a molecule as "non-self" for instance a cancer cell, they attach onto the molecule initiating the immune response, in addition, there are also accelerators and inhibitors, which provide a tight control that prevent excessive activation and autoimmune diseases, Cytotoxic T lymphocyte associated protein 4 (CTLA-4) is one of these brakes that can be manipulated to unleash the full on destruction of tumour cells by CD8 cells, there is also the programmed cell death (PD-1) molecules on T cells that interact with PD-L1 on Antigen presenting cells, by inhibiting these brakes with blocking antibodies, reduction of cancers such as metastatic melanoma can be achieved in addition to small cell carcinoma, renal carcinoma and lymphoma
