A MAJOR ROLE OF MACROPHAGE ACTIVATION BY INTERFERON-GAMMA DURING MOUSE HEPATITIS-VIRUS TYPE-3 INFECTION .2. AGE-DEPENDENT RESISTANCE

被引:16
作者
LUCCHIARI, MA
PEREIRA, CA
机构
[1] INST BUTANTAN,IMUNOL VIRAL LAB,AV DR VITAL,BRAZIL 1500,CP 65,BR-05504 SAO PAULO,BRAZIL
[2] MAX PLANCK INST IMMUNBIOL,W-7800 FREIBURG,GERMANY
基金
巴西圣保罗研究基金会;
关键词
Con A; concanavalin A; FCS; fetal calf serum; IFN; interferon; intraperitoneally; ip; lipopolysaccharide; LPS; MHV3; mouse hepatitis virus type 3; PFU; plaque forming units;
D O I
10.1016/S0171-2985(11)80163-4
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 contrast to adult mice, young AJ/mice, developed an acute hepatitis following infection with Mouse Hepatitis virus type 3. 100 % of the young animals died 4 to 5 days after the infection and high levels of virus were found in the liver and peritoneal exudate. Very low levels of IFN-$#x03B3; were found in the serum and peritoneal exudate of infected young mice. This was in contrast to the levels observed in adult mice. Spleen cells and macrophage cultures from young A/J mice, again in contrast to adult A/J mice, were shown to be unable to synthesize IFN-$#x03B3; and IFN-α/β respectively. Macrophages from either young or adult A/J mice were able to be activated with exogenous recombinant IFN-$#x03B3; or IFN-α/β, enabling both sets of cells to restrict MHV3 replication. The results indicate that the ability of the immune system to synthesize IFN-$#x03B3; and IFN-α/β may playa major role in the age-dependent resistance of A/J mice to MHV3. © 1990, Gustav Fischer Verlag · Stuttgart · New York. All rights reserved.
引用
收藏
页码:31 / 39
页数:9
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