These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: MyD88-dependent Toll-like receptor signaling is required for murine macrophages response to IS2.
    Author: Li H, Kim WJ, Jiang J, Lee SH, Youn HS, Moon EY, Kim TJ, Ye SK, Ryu JH, Kang TB, Koppula S, Park PJ, Choi DK, Lee KH.
    Journal: Int Immunopharmacol; 2011 Oct; 11(10):1578-83. PubMed ID: 21628003.
    Abstract:
    IS2, a soluble β-glucan isolated from the cell wall of mutated Saccharomyces cerevisiae (S. cerevisiae) enhances the immune response compared to the wild type (WT) β-glucan. In the present investigation we report that Toll-like receptor (TLR)/MyD88 signaling pathway was responsible in IS2 β-glucan-mediated cellular response in RAW264.7 murine macrophages. Data revealed that IS2 β-glucan significantly up-regulated the TLR2/TLR4 expression. Moreover, TLR2/TLR4 responds to IS2 resulting in murine macrophage activation. In addition, the IS2 signal led to cytokine secretions of IL-6 and TNF-α. In the case of thioglycolate-elicited peritoneal macrophages from MyD88-deficient mice, the decrease in cytokines was observed. Further the mitogen-activated protein kinases (MAPKs) phosphorylation was evident and degradation of IκB-α was increased after stimulation with IS2 β-glucan. Further examination with MyD88-deficient mice revealed that the MyD88 pathway might play an important role for IS2 β-glucan-mediated activation of macrophages.
    [Abstract] [Full Text] [Related] [New Search]