Abstract
CD95 (Fas) is known to mediate activation-induced T-cell death by apoptosis. To understand the role of CD95 during the course of bacterial infection, we examined the kinetics of αβ and γδ T cells in the peritoneal cavities and livers of 5-week-old CD95-defective MRL/lpr mice after an intraperitoneal infection with Listeria monocytogenes. The number of bacteria in the spleen decreased to an undetectable level by day 10 after infection with 7 x l03 Listeria cells similar to the number in MRL/+/+ mice. The number of αβ T cells expressing CD44 and CD95 reached a maximum in the peritoneal cavity on day 6 after listerial infection and thereafter decreased gradually in MRL/+/+ mice, whereas CD44+ αβ T cells without CD95 expression continued to increase throughout the course of listerial infection in MRL/lpr mice. Freshly isolated T cells from MRL/+/+ mice infected with L. monocytogenes 10 days previously showed DNA fragmentation with apoptosis, whereas such fragmentation was not prominent in T cells from infected MRL/lpr mice. In correlation with the increased number of CD44+ αβ T cells, Listeria-specific T-cell proliferation of peritoneal exudate cells was significantly greater in MRL/lpr mice than in MRL/+/+ mice on day l0 after listerial infection. In contrast to αβ T cells, γδ T cells increased in number only transiently in the peritoneal cavity and liver after listerial infection in both MRL/lpr mice and MRL/+/+ mice. These results suggest that CD95-mediated cell death with apoptosis may be involved in termination of the αβ-T-cell-mediated immune response after the battle against L. monocytogenes has been won, whereas γδ T cells may undergo apoptosis independently of CD95 during the course of listerial infection.
| Original language | English |
|---|---|
| Pages (from-to) | 1883-1891 |
| Number of pages | 9 |
| Journal | Infection and Immunity |
| Volume | 65 |
| Issue number | 5 |
| Publication status | Published - May 17 1997 |
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All Science Journal Classification (ASJC) codes
- Parasitology
- Microbiology
- Immunology
- Infectious Diseases
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CD95 (Fas) may control the expansion of activated T cells after elimination of bacteria in murine listeriosis. / Fuse, Y.; Nishimura, H.; Maeda, K.; Yoshikai, Y.
In: Infection and Immunity, Vol. 65, No. 5, 17.05.1997, p. 1883-1891.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - CD95 (Fas) may control the expansion of activated T cells after elimination of bacteria in murine listeriosis
AU - Fuse, Y.
AU - Nishimura, H.
AU - Maeda, K.
AU - Yoshikai, Y.
PY - 1997/5/17
Y1 - 1997/5/17
N2 - CD95 (Fas) is known to mediate activation-induced T-cell death by apoptosis. To understand the role of CD95 during the course of bacterial infection, we examined the kinetics of αβ and γδ T cells in the peritoneal cavities and livers of 5-week-old CD95-defective MRL/lpr mice after an intraperitoneal infection with Listeria monocytogenes. The number of bacteria in the spleen decreased to an undetectable level by day 10 after infection with 7 x l03 Listeria cells similar to the number in MRL/+/+ mice. The number of αβ T cells expressing CD44 and CD95 reached a maximum in the peritoneal cavity on day 6 after listerial infection and thereafter decreased gradually in MRL/+/+ mice, whereas CD44+ αβ T cells without CD95 expression continued to increase throughout the course of listerial infection in MRL/lpr mice. Freshly isolated T cells from MRL/+/+ mice infected with L. monocytogenes 10 days previously showed DNA fragmentation with apoptosis, whereas such fragmentation was not prominent in T cells from infected MRL/lpr mice. In correlation with the increased number of CD44+ αβ T cells, Listeria-specific T-cell proliferation of peritoneal exudate cells was significantly greater in MRL/lpr mice than in MRL/+/+ mice on day l0 after listerial infection. In contrast to αβ T cells, γδ T cells increased in number only transiently in the peritoneal cavity and liver after listerial infection in both MRL/lpr mice and MRL/+/+ mice. These results suggest that CD95-mediated cell death with apoptosis may be involved in termination of the αβ-T-cell-mediated immune response after the battle against L. monocytogenes has been won, whereas γδ T cells may undergo apoptosis independently of CD95 during the course of listerial infection.
AB - CD95 (Fas) is known to mediate activation-induced T-cell death by apoptosis. To understand the role of CD95 during the course of bacterial infection, we examined the kinetics of αβ and γδ T cells in the peritoneal cavities and livers of 5-week-old CD95-defective MRL/lpr mice after an intraperitoneal infection with Listeria monocytogenes. The number of bacteria in the spleen decreased to an undetectable level by day 10 after infection with 7 x l03 Listeria cells similar to the number in MRL/+/+ mice. The number of αβ T cells expressing CD44 and CD95 reached a maximum in the peritoneal cavity on day 6 after listerial infection and thereafter decreased gradually in MRL/+/+ mice, whereas CD44+ αβ T cells without CD95 expression continued to increase throughout the course of listerial infection in MRL/lpr mice. Freshly isolated T cells from MRL/+/+ mice infected with L. monocytogenes 10 days previously showed DNA fragmentation with apoptosis, whereas such fragmentation was not prominent in T cells from infected MRL/lpr mice. In correlation with the increased number of CD44+ αβ T cells, Listeria-specific T-cell proliferation of peritoneal exudate cells was significantly greater in MRL/lpr mice than in MRL/+/+ mice on day l0 after listerial infection. In contrast to αβ T cells, γδ T cells increased in number only transiently in the peritoneal cavity and liver after listerial infection in both MRL/lpr mice and MRL/+/+ mice. These results suggest that CD95-mediated cell death with apoptosis may be involved in termination of the αβ-T-cell-mediated immune response after the battle against L. monocytogenes has been won, whereas γδ T cells may undergo apoptosis independently of CD95 during the course of listerial infection.
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M3 - Article
C2 - 9125576
AN - SCOPUS:0030945162
VL - 65
SP - 1883
EP - 1891
JO - Infection and Immunity
JF - Infection and Immunity
SN - 0019-9567
IS - 5
ER -