| First Author | Funk JO | Year | 2000 |
| Journal | J Immunol | Volume | 165 |
| Issue | 9 | Pages | 4792-6 |
| PubMed ID | 11046001 | Mgi Jnum | J:119158 |
| Mgi Id | MGI:3701387 | Doi | 10.4049/jimmunol.165.9.4792 |
| Citation | Funk JO, et al. (2000) Cutting edge: resistance to apoptosis and continuous proliferation of dendritic cells deficient for TNF receptor-1. J Immunol 165(9):4792-6 |
| abstractText | The individual roles of the two TNFRs on dendritic cells (DC) are poorly understood. Investigating bone marrow-derived DC from TNFR-deficient mice, we found that cultures from TNFR1(-/-) mice continue to form proliferating clusters for 6-9 mo. In contrast, DC derived from wild-type, TNFR2(-/-), or TNFR1/2(-/-) mice survived for only 3-4 wk. DC obtained from these TNFR1(-/-) long term cultures (LTC) mice show an unusual mixed immature/mature phenotype. The continuous proliferation of the LTC is GM-CSF dependent and correlates with decreased protein levels of the cyclin-dependent kinase inhibitors p27(KIP1) and p21(CIP1). Prolonged survival of TNFR1(-/-) DC appears to be independent from NF-kappaB and Bcl-2 pathways and is rather enabled by the down-regulation of CD95, resulting in the resistance to CD95 ligand-induced apoptosis. These data point to proapoptotic signals mediated via TNFR1 and antiapoptotic signals mediated via TNFR2 in DC. |
