INTERLEUKIN-13 AND INTERLEUKIN-4 PROTECT BRONCHOALVEOLAR MACROPHAGES FROM PRODUCTIVE INFECTION WITH HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1

被引:29
作者
DENIS, M
GHADIRIAN, E
机构
[1] UNIV SHERBROOKE, FAC MED, DEPT ANAT & CELL BIOL, SHERBROOKE J1H 5N4, PQ, CANADA
[2] MONTREAL GEN HOSP, RES INST, MONTREAL H3G 1A4, PQ, CANADA
关键词
D O I
10.1089/aid.1994.10.795
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In this study, we examined the impact of the predominantly Th2-type lymphokines interleukin 13 (IL-13) and interleukin 4 (IL-4) on acute infection of human bronchoalveolar macrophages with a macrophage-tropic iso- late of human immunodeficiency virus type 1 (HIV-1). Addition of 0.01-10 ng of IL-4 or IL-13 per milliliters significantly blocked HIV-1 replication in infected cells, judging from levels of reverse transcriptase and p24 antigen in the supernatants of infected cells. Both IL-4 and IL-13 were almost as efficient as interferon-gamma (IFN-gamma) in preventing HIV-1 replication, when given in equivalent amounts. Moreover, neither IL-13 nor IL-4 interfered with the IFN-gamma-mediated enhancement of anti-HIV-1 activity in alveolar macrophages. Both IL-4 and IL-13 interfered with enhanced replication of HIV-1 in macrophages pulsed with the growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF). Interleukin 13 also prevented HIV-1 release from peripheral blood mononuclear cells in a cocultivation experiment with feeder cells from a seronegative subject. These data suggest that Th2-derived lymphokines have significant anti-HIV-1 activity in cells of the macrophage lineage, although they may enhance the susceptibility of HIV-1-infected subjects to some opportunistic pathogens.
引用
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页码:795 / 802
页数:8
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