Home Details
| Official Symbol of Gene | TNFSF10 |
| Species | Homo sapiens |
| Entrez Gene ID | 8743 |
| Official Full Name | TNF superfamily member 10 |
| Also known as | TL2; APO2L; CD253; TANCR; TRAIL; Apo-2L; TNLG6A |
| Gene Type | protein coding |
| dbXrefs | Ensembl:ENSG00000121858 MIM:603598; AllianceGenome:HGNC:11925 |
| Map Location | 3q26.31 |
| Variation Type | polymorphism |
| refSNP ID | N/A |
| Detected Sample | PBMC |
| Sample Detail | N/A |
| Detected Method | PCR-SSCP |
| Disease | MS |
| Disease subtype | RRMS, PPMS |
| Population | N/A |
| Sample Size | 123 RRMS patients / 15 PPMS patients / 125 healthy controls |
| Pubmed ID | 15020080 |
| Year | 2004 |
| Title | Identification and functional characterization of a highly polymorphic region in the human TRAIL promoter in multiple sclerosis |
| Risk Type | Disease risk |
| Main Result | Negative |
| Result | Significant differences were found neither between MS patients and healthy controls nor between different disease courses. |
| Mechanism/Pathway | Both elimination of T cells and damage to the CNS by immune cells are central pathogenic mechanisms of MS. While elimination of T cells by apoptosis is a physiological control mechanism, tissue damage in the CNS is a pathophysiological feature. During the past few years, several death receptor/ ligand systems mediating apoptosis have been discovered. We could previously show that TRAIL is able to induce massive neuronal cell destruction in the human brain.Since TRAIL receptors, but not the ligand, are expressed in the normal human brain and human antigen-specific T cells upregulate TRAIL upon activation, we expected a role of the TRAIL system in neuroinflammation. |

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