In vivo staphylococcal enterotoxin B (SEB)-primed murine splenocytes secrete mediators which suppress Cd25(hi) expression and cell cycle progression of naive splenocytes in response to SEB in vitro

Li-Jin Hsu, Ming Shiou Jan, Yee-Shin Lin

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3 Citations (Scopus)

Abstract

Administration of bacterial superantigen results in clonal activation of T cells followed by a state of hyporesponsiveness to subsequent antigen stimulation. Using a coculture system, we showed that the splenocytes from staphylococcal enterotoxin B (SEB)-injected BALB/c mice suppressed the proliferative response of naive splenocytes to SEB stimulation. The suppressive effect also occurred in Fas-deficient MRL-lpr/lpr mice. When naive responder cells were separated by a semipermeable membrane from SEB- primed effector cells, the suppressive effect remained apparent. The hyporesponsiveness of responder cells did not result from excessive induction of apoptosis, but rather from prevention of entering the S and G2/M phases of the cell cycle. The IL-2 levels in culture supernatants were low with the presence of SEB-primed effector cells. However, addition of IL-2 to the cocultures only partially reversed the inhibitory effect. Further studies revealed a reduced level of the CD25(hi) subpopulation in responder cells when cultured in the transwell with the presence of SEB-primed effector cells compared to that with saline-primed controls. This inhibitory effect was not observed for SEB-induced activation of CD25(int) and CD69 expression. Taken together, using a transwell culture system, we show in this study an inhibition of CD25(hi) expression and cell cycle arrest in target cells, which may serve at least in part the mechanisms of SEB-induced hyporesponsiveness. (C) 2000 Academic Press.

Original languageEnglish
Pages (from-to)50-57
Number of pages8
JournalCellular Immunology
Volume201
Issue number1
DOIs
Publication statusPublished - 2000 Apr 10

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Cell Cycle
Coculture Techniques
Interleukin-2
Superantigens
G2 Phase
Cell Cycle Checkpoints
In Vitro Techniques
staphylococcal enterotoxin B
Cell Division
Cultured Cells
Apoptosis
T-Lymphocytes
Antigens
Membranes

All Science Journal Classification (ASJC) codes

  • Immunology

Cite this

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title = "In vivo staphylococcal enterotoxin B (SEB)-primed murine splenocytes secrete mediators which suppress Cd25(hi) expression and cell cycle progression of naive splenocytes in response to SEB in vitro",
abstract = "Administration of bacterial superantigen results in clonal activation of T cells followed by a state of hyporesponsiveness to subsequent antigen stimulation. Using a coculture system, we showed that the splenocytes from staphylococcal enterotoxin B (SEB)-injected BALB/c mice suppressed the proliferative response of naive splenocytes to SEB stimulation. The suppressive effect also occurred in Fas-deficient MRL-lpr/lpr mice. When naive responder cells were separated by a semipermeable membrane from SEB- primed effector cells, the suppressive effect remained apparent. The hyporesponsiveness of responder cells did not result from excessive induction of apoptosis, but rather from prevention of entering the S and G2/M phases of the cell cycle. The IL-2 levels in culture supernatants were low with the presence of SEB-primed effector cells. However, addition of IL-2 to the cocultures only partially reversed the inhibitory effect. Further studies revealed a reduced level of the CD25(hi) subpopulation in responder cells when cultured in the transwell with the presence of SEB-primed effector cells compared to that with saline-primed controls. This inhibitory effect was not observed for SEB-induced activation of CD25(int) and CD69 expression. Taken together, using a transwell culture system, we show in this study an inhibition of CD25(hi) expression and cell cycle arrest in target cells, which may serve at least in part the mechanisms of SEB-induced hyporesponsiveness. (C) 2000 Academic Press.",
author = "Li-Jin Hsu and Jan, {Ming Shiou} and Yee-Shin Lin",
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T1 - In vivo staphylococcal enterotoxin B (SEB)-primed murine splenocytes secrete mediators which suppress Cd25(hi) expression and cell cycle progression of naive splenocytes in response to SEB in vitro

AU - Hsu, Li-Jin

AU - Jan, Ming Shiou

AU - Lin, Yee-Shin

PY - 2000/4/10

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N2 - Administration of bacterial superantigen results in clonal activation of T cells followed by a state of hyporesponsiveness to subsequent antigen stimulation. Using a coculture system, we showed that the splenocytes from staphylococcal enterotoxin B (SEB)-injected BALB/c mice suppressed the proliferative response of naive splenocytes to SEB stimulation. The suppressive effect also occurred in Fas-deficient MRL-lpr/lpr mice. When naive responder cells were separated by a semipermeable membrane from SEB- primed effector cells, the suppressive effect remained apparent. The hyporesponsiveness of responder cells did not result from excessive induction of apoptosis, but rather from prevention of entering the S and G2/M phases of the cell cycle. The IL-2 levels in culture supernatants were low with the presence of SEB-primed effector cells. However, addition of IL-2 to the cocultures only partially reversed the inhibitory effect. Further studies revealed a reduced level of the CD25(hi) subpopulation in responder cells when cultured in the transwell with the presence of SEB-primed effector cells compared to that with saline-primed controls. This inhibitory effect was not observed for SEB-induced activation of CD25(int) and CD69 expression. Taken together, using a transwell culture system, we show in this study an inhibition of CD25(hi) expression and cell cycle arrest in target cells, which may serve at least in part the mechanisms of SEB-induced hyporesponsiveness. (C) 2000 Academic Press.

AB - Administration of bacterial superantigen results in clonal activation of T cells followed by a state of hyporesponsiveness to subsequent antigen stimulation. Using a coculture system, we showed that the splenocytes from staphylococcal enterotoxin B (SEB)-injected BALB/c mice suppressed the proliferative response of naive splenocytes to SEB stimulation. The suppressive effect also occurred in Fas-deficient MRL-lpr/lpr mice. When naive responder cells were separated by a semipermeable membrane from SEB- primed effector cells, the suppressive effect remained apparent. The hyporesponsiveness of responder cells did not result from excessive induction of apoptosis, but rather from prevention of entering the S and G2/M phases of the cell cycle. The IL-2 levels in culture supernatants were low with the presence of SEB-primed effector cells. However, addition of IL-2 to the cocultures only partially reversed the inhibitory effect. Further studies revealed a reduced level of the CD25(hi) subpopulation in responder cells when cultured in the transwell with the presence of SEB-primed effector cells compared to that with saline-primed controls. This inhibitory effect was not observed for SEB-induced activation of CD25(int) and CD69 expression. Taken together, using a transwell culture system, we show in this study an inhibition of CD25(hi) expression and cell cycle arrest in target cells, which may serve at least in part the mechanisms of SEB-induced hyporesponsiveness. (C) 2000 Academic Press.

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