Cutting edge: resistance to apoptosis and continuous proliferation of dendritic cells deficient for TNF receptor-1
JO Funk, H Walczak, C Voigtländer… - The Journal of …, 2000 - journals.aai.org
JO Funk, H Walczak, C Voigtländer, S Berchtold, T Baumeister, P Rauch, S Rössner…
The Journal of Immunology, 2000•journals.aai.orgThe 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 …
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 …
Abstract
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-κB 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.
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