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The immune system developed certain checks and balance to control or inhibit the reactivity against normal cells of the body. Uncontrolled immune responses to the non-self entities such as bacteria, viruses, parasites, or mutated self-antigens can cause an inflammatory reaction and autoimmune diseases. To avoid an immune overreaction, the immune response is governed by a delicate balance between the expression of co-stimulatory and inhibitory signals. These signals of the immune system referred to as immune checkpoints that are crucial to maintaining the homeostasis in the body. T-cells are an important subtype of lymphocyte that plays a key role in the fighting against several diseases including cancer. Accumulation of CD8+ T cells in the tumor microenvironment (TME) directly correlates with the favorable anti-tumor responses [1]. Activated T cells express several coinhibitory receptors including programmed cell death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4). The interaction between PD-1 and its ligand PD-L1 and, CTLA4 and receptor B7 regulate T cell responses to self-proteins [2]. Expression of ligands for the checkpoint is one of the prominent mechanisms exploited by cancer cells to avoid the immune cellmediated killing which helps in their unchecked growth and progression [3]. PD-L1 expressed by tumor cells to inhibit the function and activity of T cells, whereas B7 that pairs with CTLA4 is expressed by antigen-presenting cells (APCs). Immunosuppressive TME which consists complex network of cancer cells, tumor-manipulated stromal and immune cells and soluble factors affects the functions of CD8+ T cells by inhibiting their activity or inducing apoptosis [4]. To keep the CD8+ T cells active in TME and perform their anti-tumor function, several CTLA-4 and PD-1/PD-L1 signaling axis blocking agents were developed as new immunotherapeutic tools which demonstrated huge therapeutic potential across multiple histological tumor subtypes [4,5].

CTLA-4 and PD-L1/PD-1 Pathways: Immune Checkpoint Inhibitors and Cancer Immunotherapy