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Titolo:
Tumor cell-derived TGF-beta and IL-10 dysregulate paclitaxel-induced macrophage activation
Autore:
Mullins, DW; Martins, RS; Burger, CJ; Elgert, KD;
Indirizzi:
Virginia Polytech Inst & State Univ, Dept Biol, Microbiol & Immunol Sect, Blacksburg, VA 24061 USA Virginia Polytech Inst & State Univ Blacksburg VAUSA 24061 VA 24061 USA
Titolo Testata:
JOURNAL OF LEUKOCYTE BIOLOGY
fascicolo: 1, volume: 69, anno: 2001,
pagine: 129 - 137
SICI:
0741-5400(200101)69:1<129:TCTAID>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
SEQUENCE-BINDING-PROTEIN; STABILIZING ANTINEOPLASTIC AGENT; NITRIC-OXIDE PRODUCTION; BEARING MICE; T-LYMPHOCYTES; BREAST-CANCER; TNF-ALPHA; TAXOL; PROLIFERATION; CYTOTOXICITY;
Keywords:
immunosuppression; tumor necrosis factor alpha; interleukin-12; prostaglandin E-2; nitric oxide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Elgert, KD Virginia Polytech Inst & State Univ, Dept Biol, Microbiol & Immunol Sect, Blacksburg, VA 24061 USA Virginia Polytech Inst & State Univ Blacksburg VA USA 24061 SA
Citazione:
D.W. Mullins et al., "Tumor cell-derived TGF-beta and IL-10 dysregulate paclitaxel-induced macrophage activation", J LEUK BIOL, 69(1), 2001, pp. 129-137

Abstract

Paclitaxel (TAXOL(TM)) activates in vitro macrophage (Md) expression of proinflammatory and cytotoxic mediators, including IL-12, tumor necrosis factor alpha (TNF-alpha), and nitric oxide (NO), However, tumors dysregulate Mgthrough soluble suppressor molecules, and it is possible that tumors evadepaclitaxel-mediated immune effector function through the production of immunomodulatory molecules and inhibition of Mb function in situ, Because Mb activation in the tumor microenvironment is a desirable goal of anti-tumor immunotherapy, we evaluated whether tumor-derived immunomodulatory factors dysregulate paclitaxel-mediated Mb activation. Tumor cell-derived supernatant suppressed paclitaxel's capacity to induce IL-12, TNF-alpha, and NO production by RAW264.7 Mb, Tumor factors also dysregulated paclitaxel-induced expression of a HIV-LTR, promoter-driven luciferase construct in RAW264.7 Mo,suggesting that tumors may inhibit a broad range of Mb functionality. Depletion studies revealed that IL-10 and transforming growth factor-beta (1) (TGF-beta (1)), but not prostaglandin E-2 (PGE(2)), impaired paclitaxel-mediated activation, suggesting that abrogation of these factors in situ might restore paclitaxel's activating capacity ann enhance anti-tumor efficacy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 02:42:13