The immune response is regulated by programmed cell death, or apoptosis. Death factors bind to their respective receptors and activate the apoptotic death program in target cells. A cascade of proteases called caspases mediates the apoptotic process. Loss-of-function mutations in the signaling molecules involved in apoptosis cause hyper-proliferation of cells in mouse and human. In contrast, exaggeration of this death cascade causes the destruction of various tissues. This comprehensive review explores Fas ligand-induced apoptosis, a critical process in immune regulation. In response to varied stimuli, death factors bind to their respective receptors and activate the apoptotic program in the target cell. The review highlights the significance of apoptosis in maintaining cellular homeostasis. The activated caspases cleave a variety of cellular components, a process that leads to morphological changes of the cells and nuclei, as well as to degradation of the chromosomal DNA. Dysregulation of this process has profound consequences, leading to hyper-proliferation in loss-of-function mutations and tissue destruction when the death cascade is exaggerated. Thus, a balanced apoptotic pathway is vital for proper immune function.
Published in the Annual Review of Genetics, this overview aligns with the journal's focus on providing comprehensive and up-to-date syntheses of research in genetics and related fields. By offering a detailed examination of Fas ligand-induced apoptosis, the review contributes to the broader understanding of genetic regulation of cellular processes, consistent with the journal's scope.