Apoptosis and autoimmune disease
- Author(s)
- O'Reilly, LA; Strasser, A;
- Details
- Publication Year 1999-01,Volume 48,Issue #1,Page 5-21
- Journal Title
- INFLAMMATION RESEARCH
- Publication Type
- Journal Article
- Abstract
- The process of programmed cell death or apoptosis was already noted in 1842 by Vogt [1], but it was not until the more recent studies of Kerr et al. 1972 [2] that an explosion of interest in apoptosis research occurred. Genetic, biochemical and cellular analysis in certain mammals, in the nematode Caenorhabditis elegans and in the fruitfly Drosophila melanogaster have identified several apoptosis regulating genes. This indicates that programmed cell death is an active, genetically controlled process. Many of the known cell death regulators are homologous in mammals, nematodes and insects, indicating that apoptosis is an evolutionarily conserved process. Apoptosis can be induced via multiple independent signalling pathways which converge upon a common final effector machinery. This stimulates activation of latent cysteine proteases (caspases), which cleave vital cellular substrates and thereby lead to the death of cells. The regulatory pathways of apoptosis are becoming clear with the discovery of specific signalling molecules. It has become evident that many disease processes including autoimmunity and cancer can be caused by deregulation of the apoptotic process. With the discovery of novel cell surface-bound death receptors, their ligands and further insight into the apoptotic machinery within the cell, research may ultimately lead to the design of therapies that allow intervention in the apoptotic process. The aims of such strategies would be to turn on apoptosis in neoplastic cells or in lymphocytes that are causing autoimmune disease or to prevent cell death in degenerative disorders. This review describes current understanding of the molecular regulation of apoptosis, and focuses on issues relating to possible roles of defective cell death control in autoimmunity.
- Publisher
- BIRKHAUSER VERLAG AG
- Keywords
- PROGRAMMED CELL-DEATH; TUMOR-NECROSIS-FACTOR; SYSTEMIC LUPUS-ERYTHEMATOSUS; INTERLEUKIN-1-BETA CONVERTING-ENZYME; FAS GENE-MUTATIONS; KAPPA-B ACTIVATION; SURVIVAL-PROMOTING PROTEINS; RADIATION-INDUCED APOPTOSIS; DOMAIN-CONTAINING PROTEIN; RECEPTOR TRANSGENIC MICE
- Publisher's Version
- https://doi.org/10.1007/s000110050369
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1999-01-01 12:00:00