Abstract
Treatment of guinea-pig spleen cells with glucocorticoids, such as dexamethasone (DEX), reduces concanavalin A (Con A)-induced production of chemotactic lymphokines (CLK), such as eosinophil chemotactic factor and macrophage chemotactic factor. The decreased CLK production is not caused by a direct effect of DEX on the spleen cells producing CLK, because Con A-induced CLK production is suppressed when the cells are cultured together with cell-free supernatants of the spleen cells which had been pretreated with DEX. A soluble suppressive factor, termed CLK-SF, with a MW of about 20,000, seems to be responsible for the suppression of both CLK production. CLK-SF is produced from DEX-treated T lymphocytes. CLK-SF probably exerts a critical role in the early stage of CLK production. In contrast, CLK-SF fails to inhibit Con A-induced lymphocyte proliferation, although DEX itself suppresses lymphocyte proliferation. This suggests that DEX suppresses Con A-induced CLK production by a different mechanism from that for lymphocyte proliferation.
| Original language | English |
|---|---|
| Pages (from-to) | 533-540 |
| Number of pages | 8 |
| Journal | Immunology |
| Volume | 54 |
| Issue number | 3 |
| Publication status | Published - 1985 |
| Externally published | Yes |
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Cite this
Dexamethasone suppresses concanavalin A-induced production of chemotactic lymphokines by releasing a soluble factor from splenic T lymphocytes. / Hirashima, M.; Sakata, K.; Tashiro, K.; Yoshimura, Teizo; Hayashi, H.
In: Immunology, Vol. 54, No. 3, 1985, p. 533-540.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Dexamethasone suppresses concanavalin A-induced production of chemotactic lymphokines by releasing a soluble factor from splenic T lymphocytes
AU - Hirashima, M.
AU - Sakata, K.
AU - Tashiro, K.
AU - Yoshimura, Teizo
AU - Hayashi, H.
PY - 1985
Y1 - 1985
N2 - Treatment of guinea-pig spleen cells with glucocorticoids, such as dexamethasone (DEX), reduces concanavalin A (Con A)-induced production of chemotactic lymphokines (CLK), such as eosinophil chemotactic factor and macrophage chemotactic factor. The decreased CLK production is not caused by a direct effect of DEX on the spleen cells producing CLK, because Con A-induced CLK production is suppressed when the cells are cultured together with cell-free supernatants of the spleen cells which had been pretreated with DEX. A soluble suppressive factor, termed CLK-SF, with a MW of about 20,000, seems to be responsible for the suppression of both CLK production. CLK-SF is produced from DEX-treated T lymphocytes. CLK-SF probably exerts a critical role in the early stage of CLK production. In contrast, CLK-SF fails to inhibit Con A-induced lymphocyte proliferation, although DEX itself suppresses lymphocyte proliferation. This suggests that DEX suppresses Con A-induced CLK production by a different mechanism from that for lymphocyte proliferation.
AB - Treatment of guinea-pig spleen cells with glucocorticoids, such as dexamethasone (DEX), reduces concanavalin A (Con A)-induced production of chemotactic lymphokines (CLK), such as eosinophil chemotactic factor and macrophage chemotactic factor. The decreased CLK production is not caused by a direct effect of DEX on the spleen cells producing CLK, because Con A-induced CLK production is suppressed when the cells are cultured together with cell-free supernatants of the spleen cells which had been pretreated with DEX. A soluble suppressive factor, termed CLK-SF, with a MW of about 20,000, seems to be responsible for the suppression of both CLK production. CLK-SF is produced from DEX-treated T lymphocytes. CLK-SF probably exerts a critical role in the early stage of CLK production. In contrast, CLK-SF fails to inhibit Con A-induced lymphocyte proliferation, although DEX itself suppresses lymphocyte proliferation. This suggests that DEX suppresses Con A-induced CLK production by a different mechanism from that for lymphocyte proliferation.
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UR - http://www.scopus.com/inward/citedby.url?scp=0021950315&partnerID=8YFLogxK
M3 - Article
C2 - 3871733
AN - SCOPUS:0021950315
VL - 54
SP - 533
EP - 540
JO - Immunology
JF - Immunology
SN - 0019-2805
IS - 3
ER -