Dexamethasone suppresses concanavalin A-induced production of chemotactic lymphokines by releasing a soluble factor from splenic T lymphocytes

M. Hirashima, K. Sakata, K. Tashiro, Teizo Yoshimura, H. Hayashi

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2 Citations (Scopus)

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 languageEnglish
Pages (from-to)533-540
Number of pages8
JournalImmunology
Volume54
Issue number3
Publication statusPublished - 1985
Externally publishedYes

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Lymphokines
Concanavalin A
Dexamethasone
T-Lymphocytes
Spleen
Chemotactic Factors
Lymphocytes
Eosinophil Chemotactic Factors
Glucocorticoids
Cultured Cells
Guinea Pigs

ASJC Scopus subject areas

  • Immunology

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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 journalArticle

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AU - Hirashima, M.

AU - Sakata, K.

AU - Tashiro, K.

AU - Yoshimura, Teizo

AU - Hayashi, H.

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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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