INTERFERONS ANTAGONIZE GAMMA-RAY-INDUCED DEPRESSION OF NATURAL IMMUNITY

Citation
Mp. Fuggetta et al., INTERFERONS ANTAGONIZE GAMMA-RAY-INDUCED DEPRESSION OF NATURAL IMMUNITY, International journal of radiation oncology, biology, physics, 40(4), 1998, pp. 953-960
Citations number
39
Categorie Soggetti
Oncology,"Radiology,Nuclear Medicine & Medical Imaging
ISSN journal
03603016
Volume
40
Issue
4
Year of publication
1998
Pages
953 - 960
Database
ISI
SICI code
0360-3016(1998)40:4<953:IAGDON>2.0.ZU;2-S
Abstract
Purpose: The aim of this study was to determine the inhibitory effects of in vitro radiation on the number and function of natural killer (N K) cells and to investigate the capability of interferons (IFNs) to re store the activity of NK, depressed by gamma-rays. Methods and Materia ls: Mononuclear cells (MNC) were obtained from intact or in vitro irra diated (20 Gy) peripheral blood collected from healthy donors, Alterna tively, MNC were irradiated (20 Gy) after separation from intact whole blood, The in vitro treatment of MNC with IFNs (alpha, beta, or gamma 200 UI/ml) was performed at different times after or before radiation , The NK activity (4 h-Cr-51 release test), the percentage of CD16(+)/ CD56(+) cells and apoptosis (cytometric analysis), and binding (micros copic observation) were evaluated on Days 0, 1, 2, and 5 from gamma-ra y exposure and IFNs treatment. Results: The in vitro treatment of irra diated MNC with beta IFN after radiation completely reverses the inhib itory effects of gamma-rays on human NK activity, beta IFN do not redu ce the apoptosis induction by radiation and don't modify the number of CD16- or CD56-positive cells, The binding between irradiated effecter s and tumor cells (K562) appears partially increased in beta IFN-treat ed MNC. Conclusions: The results of the present investigation suggest a possible role of beta IFN in reversing the detrimental effect of rad iation on human natural immunity and provide a rational basis for in v ivo use of beta IFN in cancer radiotherapy. (C) 1998 Elsevier Science Inc.