Basic information of Procr :
| Official Symbol of Gene | Procr |
| Species | Homo sapiens |
| Entrez Gene ID | 19124 |
| Official Full Name | protein C receptor, endothelial |
| Also known as | Ccca; Epcr; Ccd41 |
| Gene Type | protein coding |
| dbXrefs | Ensembl:ENSMUSG00000027611 AllianceGenome:MGI:104596 |
| Map Location | 2; 2 H1 |
Sample information of multiple sclerosis:
| Detected Sample | spleen |
| Sample Detail | CD4+CD62L+ T cells |
| Detected Method | RT-PCR |
| Disease | EAE |
| Disease subtype | N/A |
| Population | C57BL/6 mice |
| Sample Size | n = 5–6 mice group |
Literature information of multiple sclerosis :
| Pubmed ID | 27670590 |
| Year | 2016 |
| Title | Protein C receptor (PROCR) is a negative regulator of Th17 pathogenicity |
Results of multiple sclerosis :
| Expression | up-regulation |
| Risk type | Disease risk |
| Result | T cell–specific deficiency of PROCR resulted in the exacerbation of experimental autoimmune encephalomyelitis (EAE) and higher frequencies of Th17 cell in vivo, indicating that PROCR also inhibits pathogenicity of Th17 cells in vivo. PROCR thus does not globally inhibit Th17 responses but could be targeted to selectively inhibit proinflammatory Th17 cells |
| Mechanism/Pathway | CD4+ T cells from PROCR low expressor mutant mice readily differentiated into Th17 cells, whereas addition of the PROCR ligand, activated protein C, inhibited Th17 differentiation in vitro. In addition, PROCR acted as a negative regulator of Th17 pathogenicity in that it down-regulated expression of several pathogenic signature genes, including IL-1 and IL-23 receptors. |
