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Inhibitory activity of interleukin B on the suppressor T cell hybrid T2D4.

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Abstract Interleukin B (IL-B), a product of unstimulated B cells, is defined by its ability to selectively prevent the differentiation of suppressor T lymphocytes from precursors into effectors. The present study was undertaken to determine whether IL-B could also be active in modulating the activity of the T cell hybrid T2D4, which produces immunoglobulin-binding suppressor factors. T2D4 cells can be selectively induced by incubation with various isotypes of antibody to express isotype-specific Fc receptors and to release soluble factors that suppress production of the corresponding isotype. The data presented here demonstrate that IL-B is greatly effective in inhibiting T2D4 activities. Either pretreatment with IL-B or continuous exposure to IL-B prevents isotype activation of T2D4. As a result, T2D4 cells do not express isotype receptors and do not produce detectable amounts of isotype-specific suppressor factors. This IL-B regulatory activity on T2D4 is temperature dependent and is inhibited by cytochalasin B. These findings provide new insights on the mechanism by which IL-B enhances antibody responses, and they offer a conceptual framework for analyzing IL-B activity on suppressor T cells.
Title: Inhibitory activity of interleukin B on the suppressor T cell hybrid T2D4.
Description:
Abstract Interleukin B (IL-B), a product of unstimulated B cells, is defined by its ability to selectively prevent the differentiation of suppressor T lymphocytes from precursors into effectors.
The present study was undertaken to determine whether IL-B could also be active in modulating the activity of the T cell hybrid T2D4, which produces immunoglobulin-binding suppressor factors.
T2D4 cells can be selectively induced by incubation with various isotypes of antibody to express isotype-specific Fc receptors and to release soluble factors that suppress production of the corresponding isotype.
The data presented here demonstrate that IL-B is greatly effective in inhibiting T2D4 activities.
Either pretreatment with IL-B or continuous exposure to IL-B prevents isotype activation of T2D4.
As a result, T2D4 cells do not express isotype receptors and do not produce detectable amounts of isotype-specific suppressor factors.
This IL-B regulatory activity on T2D4 is temperature dependent and is inhibited by cytochalasin B.
These findings provide new insights on the mechanism by which IL-B enhances antibody responses, and they offer a conceptual framework for analyzing IL-B activity on suppressor T cells.

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