| http://purl.uniprot.org/citations/17785864 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17785864 | http://www.w3.org/2000/01/rdf-schema#comment | "Monocytes and monocytic cells produce proinflammatory cytokines upon direct cell contact with activated T cells. In the autoimmune disease rheumatoid arthritis, the pivotal role of TNF-alpha implies that the interaction between transmembrane TNF-alpha (mTNF) and the TNF receptors (TNFR1 and TNFR2) might participate in the T cell contact-dependent activation of monocytes. Accordingly, treatment of rheumatoid arthritis by administration of a TNF-alpha-blocking Ab was found to significantly decrease TNF-alpha production by monocytes. Several lines of evidence indicated that signaling through TNFR1/2 and through mTNF (reverse signaling) is involved in TNF-alpha production by monocytes after T cell contact: 1) blocking mTNF on activated T cells leads to a significant reduction in TNF-alpha production; 2) down-regulation of TNFR1/2 on monocytes by transfection with small interfering RNA results in diminished TNF-alpha production; 3) blocking or down-regulating TNFR2 on activated T cells inhibits TNF-alpha production, indicating that mTNF on the monocyte surface mediates signaling; 4) ligation of mTNF on monocytes by surface TNFR2 transfected into resting T cells induces TNF-alpha production due to reverse signaling by mTNF; and 5) ligation of mTNF on monocytes by a soluble TNFR2:Ig receptor construct induces TNF-alpha production due to reverse signaling. In conclusion, we identified mTNF and TNFR1/2 as interaction partners contributing to TNF-alpha production in monocytes. Both pathways initiated by mTNF-TNFR interaction are likely to be inhibited by treatment with anti-TNF-alpha Abs."xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.179.6.4239"xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/author | "Wagner U."xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/author | "Hauschildt S."xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/author | "Hantzschel H."xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/author | "Pierer M."xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/author | "Kaltenhauser S."xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/author | "Meusch U."xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/author | "Rossol M."xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/pages | "4239-4248"xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/title | "Interaction between transmembrane TNF and TNFR1/2 mediates the activation of monocytes by contact with T cells."xsd:string |
| http://purl.uniprot.org/citations/17785864 | http://purl.uniprot.org/core/volume | "179"xsd:string |
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