Abstract
Several studies have suggested that activation-induced apoptosis of Ag- specific CD4+ T cells leads to depletion of this subset during HIV infection. The bacterial superantigen, staphylococcal enterotoxin A (SEA), is known to induce activation-induced apoptosis in the TCR Vβ-bearing CD4+ T cells in the periphery after clonal expansion of these cells. The murine retroviral model of AIDS (MAIDS), which is induced by LP-BM5 murine leukemia virus, shares many common features with HIV infection in humans, except that CD4+ T cells increase progressively in susceptible strains. In this study, we challenged SEA to MAIDS mice and examined whether this retrovirus affects the fate of the SEA-reactive CD4+ T cells in vivo. At 4 wk post-infection with LP-BM5 murine leukemia virus, clonal expansion and subsequent deletion of SEA-reactive CD4+Vβ3+ T cells occurred normally after SEA administration, whereas in vitro proliferative responses were severely impaired. At 8 wk postinfection, the in vivo expansion of CD4+Vβ3+ T cells was evident, but not followed by clonal deletion, as late as 14 days after SEA administration. This expanding subset in the infected mice expressed the Fas Ag in the same amount as the same subset in uninfected controls. These findings suggest that activation-induced apoptosis of superantigen-reactive CD4+ T cells is interfered with in vivo during the course of MAIDS, which is not attributable to underexpression of the Fas Ag by the CD4+ T cells.
| Original language | English |
|---|---|
| Pages (from-to) | 3611-3621 |
| Number of pages | 11 |
| Journal | Journal of Immunology |
| Volume | 153 |
| Issue number | 8 |
| Publication status | Published - Oct 15 1994 |
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All Science Journal Classification (ASJC) codes
- Immunology and Allergy
- Immunology
Cite this
Clonal expansion but lack of subsequent clonal deletion of bacterial superantigen-reactive T cells in murine retroviral infection. / Aoki, Yoshiyasu; Hiromatsu, Kenji; Usami, Jun; Makino, Masahiko; Igarashi, Hideo; Ogasawara, Jun; Nagata, Shigekazu; Yoshikai, Yasunobu.
In: Journal of Immunology, Vol. 153, No. 8, 15.10.1994, p. 3611-3621.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Clonal expansion but lack of subsequent clonal deletion of bacterial superantigen-reactive T cells in murine retroviral infection
AU - Aoki, Yoshiyasu
AU - Hiromatsu, Kenji
AU - Usami, Jun
AU - Makino, Masahiko
AU - Igarashi, Hideo
AU - Ogasawara, Jun
AU - Nagata, Shigekazu
AU - Yoshikai, Yasunobu
PY - 1994/10/15
Y1 - 1994/10/15
N2 - Several studies have suggested that activation-induced apoptosis of Ag- specific CD4+ T cells leads to depletion of this subset during HIV infection. The bacterial superantigen, staphylococcal enterotoxin A (SEA), is known to induce activation-induced apoptosis in the TCR Vβ-bearing CD4+ T cells in the periphery after clonal expansion of these cells. The murine retroviral model of AIDS (MAIDS), which is induced by LP-BM5 murine leukemia virus, shares many common features with HIV infection in humans, except that CD4+ T cells increase progressively in susceptible strains. In this study, we challenged SEA to MAIDS mice and examined whether this retrovirus affects the fate of the SEA-reactive CD4+ T cells in vivo. At 4 wk post-infection with LP-BM5 murine leukemia virus, clonal expansion and subsequent deletion of SEA-reactive CD4+Vβ3+ T cells occurred normally after SEA administration, whereas in vitro proliferative responses were severely impaired. At 8 wk postinfection, the in vivo expansion of CD4+Vβ3+ T cells was evident, but not followed by clonal deletion, as late as 14 days after SEA administration. This expanding subset in the infected mice expressed the Fas Ag in the same amount as the same subset in uninfected controls. These findings suggest that activation-induced apoptosis of superantigen-reactive CD4+ T cells is interfered with in vivo during the course of MAIDS, which is not attributable to underexpression of the Fas Ag by the CD4+ T cells.
AB - Several studies have suggested that activation-induced apoptosis of Ag- specific CD4+ T cells leads to depletion of this subset during HIV infection. The bacterial superantigen, staphylococcal enterotoxin A (SEA), is known to induce activation-induced apoptosis in the TCR Vβ-bearing CD4+ T cells in the periphery after clonal expansion of these cells. The murine retroviral model of AIDS (MAIDS), which is induced by LP-BM5 murine leukemia virus, shares many common features with HIV infection in humans, except that CD4+ T cells increase progressively in susceptible strains. In this study, we challenged SEA to MAIDS mice and examined whether this retrovirus affects the fate of the SEA-reactive CD4+ T cells in vivo. At 4 wk post-infection with LP-BM5 murine leukemia virus, clonal expansion and subsequent deletion of SEA-reactive CD4+Vβ3+ T cells occurred normally after SEA administration, whereas in vitro proliferative responses were severely impaired. At 8 wk postinfection, the in vivo expansion of CD4+Vβ3+ T cells was evident, but not followed by clonal deletion, as late as 14 days after SEA administration. This expanding subset in the infected mice expressed the Fas Ag in the same amount as the same subset in uninfected controls. These findings suggest that activation-induced apoptosis of superantigen-reactive CD4+ T cells is interfered with in vivo during the course of MAIDS, which is not attributable to underexpression of the Fas Ag by the CD4+ T cells.
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UR - http://www.scopus.com/inward/citedby.url?scp=0028061857&partnerID=8YFLogxK
M3 - Article
C2 - 7523498
AN - SCOPUS:0028061857
VL - 153
SP - 3611
EP - 3621
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 8
ER -