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Th0‐like CD4 + T cells protect mice with murine retrovirus‐induced immunodeficiency syndrome (MAIDS) against co‐infection with Listeria monocytogenes
Author(s) -
HIROMATSU K.,
NISHIMURA H.,
KIMURA K.,
AOKI Y.,
USAMI J.,
KOBAYASHI N.,
MAKINO M.,
YOSHIKAI Y.
Publication year - 1996
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1996.d01-769.x
Subject(s) - listeria monocytogenes , listeria , biology , microbiology and biotechnology , listeria infection , immune system , virology , immunodeficiency , immunity , immunology , bacteria , genetics
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 + αβ T cells but neither by γδ T cells nor natural killer (NK) cells. Interferon‐γ (IFN‐γ) 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‐γ 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.