Immune Check point proteins and Immunosupressive Drugs Melanoma: Nivolumab, and Ipilimumab
NSCLC Renal cell cancer Advanced Urothelial Cancer Head and neck cancer PDL1, CCS4, Treg, IFN , IL 2, Ipilimumab, Lymphoma Leukemia Previously: IFN Alpha-2b, IL-2, BCG IFN for solid tumors IFN for RCC IFN for Melanoma IL-2 Activated T cell secrete it. Stimulates LAKs (Lymphocyte-Lymphokines-activated Killer Cells)       Cancer takes advantage of the ability to hide from the immune system by explotting a series of immune escape mechanisms
that were developed to avoid autoimmunity. Among these mechanisms are the hijacking of
immune-cell intrinsic checkpoints that are induced on T-cell activation. CTLA-4 (cytotoxic
T-lymphocyte–associated antigen 4) is one of such check point. Ipilimumab is an antibody, that binds to CTLA-4 and thus derepresses the T cell activation. Thus, T-cell get activated. 2nd mechanism that Cancer cell uses to protect themselves is by making T cell functionally non-active after prolonged exposure to T cell. They do so by causing expression of PD-1 (Progamemed death 1) receptor in T cell and they them selves generate PD-1 Ligand that binds to such receptor to make T cell inactive. This in turn suppresses the effect of TCR on T cell activation. Thus, T cell remains inactive. Blockade of PD-1 or PD-1 Ligand helps T cell remain active. Yet to Read: |
Clinical Immunology >
