English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Interleukin (IL)-18 has been well characterized as a costimulatory factor for the induction of IL-12-mediated interferon (IFN)-gamma production by T helper (Th)1 cells, but also can induce IL-4 production and thus facilitate the differentiation of Th2 cells. To determine the mechanisms by which IL-18 might regulate these diametrically distinct immune responses, we have analyzed the role of cytokines in the regulation of IL-18 receptor alpha chain (IL-18Ralpha) expression. The majority of peripheral CD4(+) T cells constitutively expressed the IL-18Ralpha. Upon antigen stimulation in the presence of IL-12, marked enhancement of IL-18Ralpha expression was observed. IL-12-mediated upregulation of IL-18Ralpha required IFN-gamma. Activated CD4(+) T cells that expressed low levels of IL-18Ralpha could produce IFN-gamma when stimulated with the combination of IL-12 and IL-18, while CD4(+) cells which expressed high levels of IL-18Ralpha could respond to IL-18 alone. In contrast, T cell stimulation in the presence of IL-4 resulted in a downregulation of IL-18Ralpha expression. Both IL-4(-/)- and signal transducer and activator of transcription (Stat)6(-/)- T cells expressed higher levels of IL-18Ralpha after TCR stimulation. Furthermore, activated T cells from Stat6(-/)- mice produced more IFN-gamma in response to IL-18 than wild-type controls. Thus, positive/negative regulation of the IL-18Ralpha by the major inductive cytokines (IL-12 and IL-4) determines the capacity of IL-18 to polarize an immune response.

Regulation of Interleukin (Il)-18 Receptor α Chain Expression on Cd4+ T Cells during T Helper (Th)1/Th2 Differentiation