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Modulation of Life and Death by the TNF Receptor Superfamily

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Modulation of Life and Death by the TNF Receptor Superfamily Oncogene (1998) 17, 3261 ± 3270 ã 1998 Stockton Press All rights reserved 0950 ± 9232/98 $12.00 http://www.stockton-press.co.uk/onc Modulation of life and death by the TNF receptor superfamily Stacey J Baker*,1 and E Premkumar Reddy1 1Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, 3307 N Broad Street, Philadelphia, Pennsylvania 19140, USA The tumor necrosis factor receptor (TNFR) superfamily Cell death is thought to occur by two mechanisms, represents a growing family, with over 20 members necrosis and apoptosis. While necrosis is believed to having been identi®ed thus far in mammalian cells. These occur in response to physical injury, apoptosis, or proteins share signi®cant homologies in their extracel- programmed cell death, is a genetically encoded and lular ligand binding domains and intracellular eector tightly regulated `suicidal' process in which the cell (death) domains. These receptors appear to transmit actively participates in its own destruction. Apoptosis their signals via protein-protein interactions, which is morphologically characterized by membrane bleb- convey either a death or survival signal. Isolation and bing, cytoplasmic, nuclear and chromatin condensa- characterization of death domain containing proteins tion, and DNA fragmentation. The cell ultimately (TRADD, FADD/MORT-1, RIP), TRAF domain collapses into distinct apoptotic bodies of condensed containing proteins (TRAF1-6) as well as new members chromatin with intact membranes that display speci®c and adaptor proteins such as DAXX have provided new surface markers which direct neighboring phagocytic insights to our understanding of signaling mechanisms cells to engulf the vesicles before they rupture and associated with this family of receptors. While the death subsequently trigger an undesired in¯ammatory im- signals seem to be associated with the activation of both mune response (reviewed in Martin et al., 1994; White, the caspase and JUN kinase pathways, the survival 1995). Some of these stimuli, such as tumor necrosis signals are mediated via the activation of the NF-kB factor (TNF) and some of its relatives, can provide pathway. suicidal signals via proteins containing a `death domain', while others, such as transforming growth Keywords: TNFR; death domain; apoptosis; TRAF; factor beta (TGF-b) are potent and rapid inhibitors of TRADD; FADD; DAXX; ASK; JNK; NF-kB proliferation and inducers of growth arrest and apoptosis (reviewed in Homan and Liebermann, 1994; Arch et al., 1998; Ashkenazi and Dixit, 1998). Regulation of apoptosis is genetically controlled by Introduction numerous genes, some of which have remained highly conserved throughout evolution. The continued replenishment of the cellular compo- nents which comprise the hematopoietic system is dependent upon a culmination of signaling events Genetic regulators of apoptosis which instruct uncommitted pluripotent stem cells to proliferate and subsequently commit themselves to Genetic regulation of apoptosis has been best studied dierentiate along the myeloid, lymphoid or erythroid in the nematode Caenothabditis elegans (C. elegans), lineages. Environmental factors such as the bone where it has been possible to isolate mutants that are marrow microenvironment and cellular responsiveness defective in various aspects of programmed cell death. to interleukins and cytokines were once thought to Among the 1090 cells generated during the develop- govern the establishment and maintenance of each ment of C. elegans, there are 131 cells that undergo hematopoietic lineage. Presumably, by `permitting' programmed cell death and the timing and identities of these soluble factors to dictate whether a cell will these cells are invariant in individual worms. Since the continue to remain in a resting state, proliferate, or body of C. elegans is transparent during embryonic terminally dierentiate, the individual constituents of development, it has been possible to observe the cells the hematopoietic system are delicately and critically undergoing apoptosis using microscopic techniques balanced in both cell type and number (Wyllie et al., such as Nomarsi optics. Genetic analysis of mutants 1980; Williams et al., 1992; Williams and Smith, 1993). of C. elegans that are defective in programmed cell Disruptions in this physiological balance are clinically death has identi®ed a set of genes which act as positive manifested in several disease states, including cancer, in and negative regulators of this biological process. which the developmental and proliferative constraints Recent studies have shown that several of the genes that are normally placed upon a developing cell are that regulate the apoptotic pathways of C. elegans are ignored. To avoid the onset of such defects in cellular highly conserved throughout evolution and counter- development, cells utilize their capability to respond to parts for these genes can be readily detected in humans additional stimuli which trigger the activation of (Steller, 1995; Yuan, 1996). `suicidal' signal transduction pathways. One of the important genes identi®ed in C. elegans by this type of genetic analysis is Ced-9, in which a dominant gain of function mutation suppresses all normal programmed cell death, while recessive loss-of- function mutation causes apoptosis in many normally *Correspondence: SJ Baker living cells leading to the death of the organism. Signal transduction by TNFR superfamily SJ Baker and EP Reddy 3262 Studies with this gene in C. elegans suggest that the with which the ligands bind to their cognate receptors. product of ced-9 acts as a gatekeeper of apoptosis, In contrast to other protein families with notable where downregulation of this gene is necessary for cells homology, each of these family members displays no to undergo programmed cell death (Yuan, 1996). more than 20 ± 25% homology (which is found mostly Cloning and molecular characterization of ced-9 in the extracellular region) at the protein level. showed that it codes for a protein of 280 amino Although these proteins, for the most part, exist as acids, which is homologous to the mammalian protein trimeric or multimeric membrane bound proteins which bcl-2 (Tsujimoto et al., 1985; reviewed in Yuan, 1996; function to induce receptor aggregation, there are a few Adams and Cory, 1998). members, such as TNF and FasL, which are functional Two other genes which appear to be essential for the in a soluble form. Regardless of conformation, these programmed cell death of C. elegans are ced-3 and ced- ligands, in a mechanism analogous to other cytokines 4 (reviewed in Yuan, 1996; Adams and Cory, 1998). and growth factors, exert their eects through receptor- Loss of function mutations in these two genes abolish ligand interactions which induce downstream signal the programmed cell death of all 131 cells during C. transduction events (Gruss and Dower, 1995). elegans hermaphrodite development. The ced-4 gene There are slightly more members of the TNF codes for a 549 amino acid protein which contains two receptor (TNFR) superfamily as there are ligands regions that contains two calcium binding domain with which they interact: TNF-RI (p55), TNF-RII known as the EF-hand. The ced-3 gene, on the other (p75), TNF-RIII (TNF-RP) , OX-40, 4-1BB, CD40, hand, codes for a protein of 503 amino acids which CD30, CD27, the poxvirus gene products PV-T2 and and was originally thought to be homologous to PV-A53R, and p75 NGFR, CAR1, DR3 (also known caspase-1 (Yuan et al., 1993), a cysteine protease as APO3, WSL-1, TRAMP, LARD), DR4, DR5 (also which processes interleukin-1b (IL-1b) into a mature known as APO2, TRAIL-R2, TRICK 2 or KILLER) and functional form that is required during an (Smith et al., 1993; Armitage, 1994; Gruss and Dower, in¯ammatory response (Salvesen and Dixit, 1997; 1995; Ashkenazi and Dixit, 1998). One of the most Thornberry and Lazebnik, 1998). notable additions to this list is the p75 low anity Apoptotic machinery is normally suppressed or nerve growth factor receptor (NGFR). While this activated by signals from the extracellular environ- protein was actually the ®rst family member to be ment as well as intracellular sensors that monitor DNA identi®ed, its low-anity ligand is structurally un- damage. The absence of external survival signals or related to the TNF ligands and is therefore not irreparable DNA damage are some of the important included as a member of the ligand superfamily. events that appear to trigger apoptosis in lower Almost as notable are the PV-T2 and PV-A53R pox organisms such as C. elegans. While preserving these virus gene products which encode soluble homologs of apoptotic responses, higher organisms such as mam- the TNF receptors. The mammalian TNFR family mals have evolved a distinctive mechanism that enables members are type I membrane proteins and, in spite of the organism to instruct certain cell populations to their low degree of homology (20 ± 25%), are grouped enter apoptotic pathways at dierent stages of together as such due to the presence of conserved development. This is well exempli®ed in the case of cysteine residues in the extracellular ligand-binding immune system, where it is necessary to eliminate the domain. In general, each receptor contains varying presence of T and B cell populations following their numbers of cysteine rich domains (CRDs), each of expansion in response to external infection (Boise and which is characterized by the presence of approxi- Thompson, 1996; Winoto, 1997). To achieve this, mately
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