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Titolo:
Paclitaxel enhances macrophage IL-12 production in tumor-bearing hosts through nitric oxide
Autore:
Mullins, DW; Burger, CJ; Elgert, KD;
Indirizzi:
Virginialacksburg,Inst & State Univ, Microbiol & Immunol Sect, Dept Biol, B Virginia Polytech Inst & State Univ Blacksburg VA USA 24061 Dept Biol, B
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 11, volume: 162, anno: 1999,
pagine: 6811 - 6818
SICI:
0022-1767(19990601)162:11<6811:PEMIPI>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERFERON-GAMMA PRODUCTION; CELL STIMULATORY FACTOR; NECROSIS-FACTOR-ALPHA; STABILIZING ANTINEOPLASTIC AGENT; IFN-GAMMA; MEDIATED SUPPRESSION; TYROSINE PHOSPHORYLATION; PERITONEAL-MACROPHAGES; MURINE MACROPHAGES; ANTITUMOR-ACTIVITY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
70
Recensione:
Indirizzi per estratti:
Indirizzo: Elgert, KD Virginia119lytech Inst & State Univ, Microbiol & Immunol Sect, Dept Biol, 2 Virginia Polytech Inst & State Univ 2119 Derring Hall Blacksburg VA USA 24061
Citazione:
D.W. Mullins et al., "Paclitaxel enhances macrophage IL-12 production in tumor-bearing hosts through nitric oxide", J IMMUNOL, 162(11), 1999, pp. 6811-6818

Abstract

Tumor-induced macrophages (M phi s) mediate immunosuppression, in part, through increased production of factors that suppress T cell responsiveness and underproduction of positive regulatory cytokines, Pretreatment of tumor-bearing host (TBH) M phi s with the anticancer agent paclitaxel (Taxol) partially reverses tumor-induced M phi suppressor activity, suggesting that paclitaxel may restore TBH M phi production of proimmune factors. Because paclitaxel demonstrates LPS-mimetic capabilities and increased production of the LPS-induced immunostimulatory cytokine IL-12 could account for enhanced T cell responsiveness, we investigated whether paclitaxel induces M phi IL-12 production. Tumor growth significantly down-regulated M phi IL-12 p70 production through selective dysregulation of IL-12 p40 expression. LPS stimulation failed to overcome tumor-induced dysregulation of p40 expression. Incontrast, paclitaxel significantly enhanced both normal host and TBH M phiIL-12 p70 production in vitro, although TBH M phi IL-12 production was lower than that of similarly treated normal host M phi s. Paclitaxel enhanced p40 expression in a dose-dependent manner. Through reconstituted M phi IL-12 expression, paclitaxel pretreatment relieved tumor-induced M phi suppression of T cell alloreactivity. Blocking M phi NO suppressed paclitaxel's ability to induce IL-12 production. This suggests that paclitaxel;induced activities may involve a NO-mediated autocrine induction pathway. Collectively,these data demonstrate that paclitaxel restores IL-12 production in the TBH and ascribe a novel immunotherapeutic component to the pleiotropic activities of NO, Through its capacity to induce IL-12 production, paclitaxel maycontribute to the correction of tumor-induced immune dysfunction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/07/20 alle ore 19:23:46