Blausen Medical
Blausen Medical

Blausen Medical

Medically accurate and informative 3D animations



The immune system has the ability to detect and destroy tumor cells through activated T cells and other mechanisms. The first step involves the recognition of tumor cells by the immune system. The genetic alterations that accumulate in tumor cells can lead to the expression of tumor-specific antigens that are not expressed in normal tissue. The antigenic peptides produced by tumor cells are captured by antigen-presenting cells, known as dendritic cells. The dendritic cells then migrate back to the secondary lymph organs, including the lymph nodes, where they present the tumor-derived antigenic peptides to naïve T cells, resulting in their differentiation and maturation into helper T cells and cytotoxic T cells. Antigen-specific cytotoxic T cells are activated and migrate back to the tumor to kill the tumor cells through a variety of antitumor effector mechanisms. This process is a component of the adaptive antitumor immune response. However, some tumors may exploit various immune pathways to avoid detection by T cells. One of these pathways is the programmed death receptor-1, also known as PD-1. PD-1 is an inhibitory receptor expressed on T cells after activation, and is referred to as an “immune checkpoint,” since it serves to regulate the amplitude and quality of the T cell response. The normal physiologic function of immune checkpoints is to modulate the intensity of T cell activity during an inflammatory response to infection, in order to limit autoimmunity and collateral tissue damage. After a T cell has been activated by an antigen, PD-1 becomes upregulated. PD-1 has 2 cognate ligands: PD-L1 and PD-L2. The interaction of PD-1 with its ligands can downregulate T cell activity. Binding of the PD-1 ligands to the PD-1 receptor found on T cells inhibits T cell proliferation and cytokine production. Upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway can contribute to inhibition of active T cell immune surveillance of tumors. Let’s see how KEYTRUDA activates the antitumor immune response. KEYTRUDA is a humanized monoclonal antibody that binds to the PD-1 receptor and blocks its interaction with PD-L1 and PD-L2. Keeping in mind that a cytotoxic T cell becomes inactivated through the interaction of the PD-1 receptor and one of its ligands, KEYTRUDA prevents this from happening by blocking the PD-1 receptor, resulting in the continued activation of the cytotoxic T cell, thereby releasing the PD-1 pathway-mediated inhibition of the immune response, including the antitumor response. While having an effect on the tumor cell, this could also affect normal, healthy cells.

Duration: 03:46
Licence: CC - Attribution
Original Language: English
Published: 8/9/2019
Diseases and Conditions: Lung Cancer
Format: 3D Animation

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