Abstract
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 C57BL16 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.
| Original language | English |
|---|---|
| Pages (from-to) | 532-538 |
| Number of pages | 7 |
| Journal | Immunology |
| Volume | 89 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Jan 1 1996 |
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All Science Journal Classification (ASJC) codes
- Immunology and Allergy
- Immunology
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Th0-like CD4+ T cells protect mice with murine retrovirus-induced immunodeficiency syndrome (MAIDS) against co-infection with Listeria monocytogenes. / Hiromatsu, K.; Nishimura, H.; Kimura, K.; Aoki, Y.; Usami, J.; Kobayashi, N.; Makino, M.; Yoshikai, Y.
In: Immunology, Vol. 89, No. 4, 01.01.1996, p. 532-538.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Th0-like CD4+ T cells protect mice with murine retrovirus-induced immunodeficiency syndrome (MAIDS) against co-infection with Listeria monocytogenes
AU - Hiromatsu, K.
AU - Nishimura, H.
AU - Kimura, K.
AU - Aoki, Y.
AU - Usami, J.
AU - Kobayashi, N.
AU - Makino, M.
AU - Yoshikai, Y.
PY - 1996/1/1
Y1 - 1996/1/1
N2 - 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 C57BL16 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.
AB - 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 C57BL16 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=0029958084&partnerID=8YFLogxK
U2 - 10.1046/j.1365-2567.1996.d01-769.x
DO - 10.1046/j.1365-2567.1996.d01-769.x
M3 - Article
C2 - 9014817
AN - SCOPUS:0029958084
VL - 89
SP - 532
EP - 538
JO - Immunology
JF - Immunology
SN - 0019-2805
IS - 4
ER -