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Titolo:
Cutting edge: Resistance to apoptosis and continuous proliferation of dendritic cells deficient for TNF receptor-1
Autore:
Funk, JO; Walczak, H; Voigtlander, C; Berchtold, S; Baumeister, T; Rauch, P; Rossner, S; Steinkasserer, A; Schuler, G; Lutz, MB;
Indirizzi:
Univ Erlangen Nurnberg, Dept Dermatol, D-91052 Erlangen, Germany Univ Erlangen Nurnberg Erlangen Germany D-91052 -91052 Erlangen, Germany German Canc Res Ctr, Tumor Immunol Program, D-6900 Heidelberg, Germany German Canc Res Ctr Heidelberg Germany D-6900 D-6900 Heidelberg, Germany
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 9, volume: 165, anno: 2000,
pagine: 4792 - 4796
SICI:
0022-1767(20001101)165:9<4792:CERTAA>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; COLONY-STIMULATING FACTOR; MOUSE BONE-MARROW; LANGERHANS CELLS; DOWN-REGULATION; IN-VIVO; GM-CSF; ALPHA; MICE; DIFFERENTIATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Lutz, MB Univ Erlangen Nurnberg, Dept Dermatol, Hartmannstr 14, D-91052 Erlangen, Germany Univ Erlangen Nurnberg Hartmannstr 14 Erlangen Germany D-91052 y
Citazione:
J.O. Funk et al., "Cutting edge: Resistance to apoptosis and continuous proliferation of dendritic cells deficient for TNF receptor-1", J IMMUNOL, 165(9), 2000, pp. 4792-4796

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 tohe 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 TNFR1and antiapoptotic signals mediated via TNFR2(-/-) in DC.

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Documento generato il 26/11/20 alle ore 20:22:47