Th0-like CD4(+) T cells protect mice with murine retrovirus-induced immunodeficiency syndrome (MAIDS) against co-infection with Listeria monocytogenes

被引:2
|
作者
Hiromatsu, K
Nishimura, H
Kimura, K
Aoki, Y
Usami, J
Kobayashi, N
Makino, M
Yoshikai, Y
机构
[1] NAGOYA UNIV,SCH MED,HOST DEF LAB,DIS MECHANISM & CONTROL RES INST,SHOWA KU,NAGOYA,AICHI 466,JAPAN
[2] KAGOSHIMA UNIV,FAC MED,CTR CHRON VIRAL DIS,DIV HUMAN RETROVIRUS,KAGOSHIMA 890,JAPAN
关键词
D O I
10.1046/j.1365-2567.1996.d01-769.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We examined the host defence mechanism against infection with Listeria monocytogenes, a facultative intracellular bacterium, in mice with murine acquired immunodeficiency syndrome (MAIDS) caused by LP-BM5 murine leukaemia virus (MuLv) infection. Although LP-BM5 MuLV infection in C57BL/6 mice leads to a stage of immunodeficiency characterized by severe compromise of cell-mediated immunity, the mice with established MAIDS infected with LP-BM5 8 weeks previously, showed resistance to an intraperitoneal infection with Listeria monocytogenes. These MAIDS mice also showed resistance to a lethal dose of secondary listerial challenge, while the delayed-type hypersensitivity response to heat-killed Listeria (HKL) was severely impaired in MAIDS mice. The resistance of MAIDS mice to listerial infection was mediated by CD4(+) alpha beta T cells but neither by gamma delta T cells nor natural killer (NK) cells. Interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) were produced by CD4(+) T cells from Listeria-infected MAIDS mice in response to the in vitro stimulation with HKL, whereas IFN-gamma but not IL-10 were produced by those from Listeria-infected control mice. These results suggest that T-helper 0 (Th0)-like immune responses of CD4(+) T cells occur and participate in host defence mechanisms against listerial infection in MAIDS mice.
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页码:532 / 538
页数:7
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