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Titolo:
INTERLEUKIN-12 OVERCOMES PACLITAXEL-MEDIATED SUPPRESSION OF T-CELL PROLIFERATION
Autore:
MULLINS DW; KOCI MD; BURGER CJ; ELGERT KD;
Indirizzi:
VIRGINIA POLYTECH INST & STATE UNIV,DEPT BIOL,MICROBIOL & IMMUNOL SECT BLACKSBURG VA 24061 VIRGINIA POLYTECH INST & STATE UNIV,DEPT BIOL,MICROBIOL & IMMUNOL SECT BLACKSBURG VA 24061
Titolo Testata:
Immunopharmacology and immunotoxicology
fascicolo: 4, volume: 20, anno: 1998,
pagine: 473 - 492
SICI:
0892-3973(1998)20:4<473:IOPSOT>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
NECROSIS-FACTOR-ALPHA; STABILIZING ANTINEOPLASTIC AGENT; MACROPHAGE NITRIC-OXIDE; TUMOR-BEARING MICE; ACTIVATED LYMPHOCYTES; ANTITUMOR-ACTIVITY; STIMULATORY FACTOR; INNATE RESISTANCE; ADAPTIVE IMMUNITY; INTERFERON-GAMMA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
61
Recensione:
Indirizzi per estratti:
Citazione:
D.W. Mullins et al., "INTERLEUKIN-12 OVERCOMES PACLITAXEL-MEDIATED SUPPRESSION OF T-CELL PROLIFERATION", Immunopharmacology and immunotoxicology, 20(4), 1998, pp. 473-492

Abstract

The antineoplastic agent paclitaxel (TAXOL(TM)) is a potent inhibitorof tumor cell division and a useful chemotherapeutic for the treatment of refractory ovarian and breast carcinoma. Multiple immune system actions have been ascribed to paclitaxel, including the capacity to induce macrophage antitumor cytotoxic molecule production. However, T-cells are susceptible to paclitaxel's cytostatic functions, and no studies have investigated the effects of direct paclitaxel administration onlymphocyte function in the tumor-bearing host (TBH). Because paclitaxel is currently used as an antitumor chemotherapeutic agent and tumor growth alters leukocyte functions, we assessed T-cell function following chemotherapeutic-type paclitaxel treatment. Paclitaxel administration significantly compromised the proliferative capacity of both normalhost and TBH lymphocytes in vitro. Although tumor growth impaired T-cell interferon-gamma (IFN-gamma) production, paclitaxel treatment did not alter IFN-gamma. We speculate that the immunostimulatory cytokine interleukin-12 (IL-12), which promoted T-cell activation and proliferation, was capable of reversing paclitaxel-mediated immunosuppression. Exogenous IL-12 fully reconstituted proliferative reactivity and enhanced IFN-gamma production by both normal host and TBH lymphocytes in vitro. Collectively, these data suggest that chemotherapeutic paclitaxelregimens impart significant but reversible inhibition of lymphocyte populations, and IL-12 may be a useful ancillary immunotherapeutic to overcome paclitaxel-induced modulation of lymphocyte activities.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/08/20 alle ore 23:22:09