World Library  


Add to Book Shelf
Flag as Inappropriate
Email this Book

Plos One : Toll-like Receptor 2 and Toll-like Receptor 4-dependent Activation of B Cells by a Polysaccharide from Marine Fungus Phoma Herbarum Ys4108, Volume 8

By Lafrenie, Robert

Click here to view

Book Id: WPLBN0003968764
Format Type: PDF eBook :
File Size:
Reproduction Date: 2015

Title: Plos One : Toll-like Receptor 2 and Toll-like Receptor 4-dependent Activation of B Cells by a Polysaccharide from Marine Fungus Phoma Herbarum Ys4108, Volume 8  
Author: Lafrenie, Robert
Volume: Volume 8
Language: English
Subject: Journals, Science, Medical Science
Collections: Periodicals: Journal and Magazine Collection (Contemporary)
Historic
Publication Date:
Publisher: Plos

Citation

APA MLA Chicago

Lafrenie, R. (n.d.). Plos One : Toll-like Receptor 2 and Toll-like Receptor 4-dependent Activation of B Cells by a Polysaccharide from Marine Fungus Phoma Herbarum Ys4108, Volume 8. Retrieved from http://netlibrary.net/


Description
Description : Various natural polysaccharides are capable of activating the immune system and therefore can be employed as biological response modifiers in anti-tumor therapy. We previously found a homogenous polysaccharide from the mycelium of marine fungus Phoma herbarum YS4108, named YCP, exhibiting strong in vivo antitumor ability via enhancement of the host immune responses. To further elucidate the role of YCP as a biological response modifier, the immunomoduating activities of YCP in B cells was investigated in the current study. We demonstrated that stimulation of YCP with murine splenic B cells resulted in cell proliferation and generation of IgM antibody response. Binding of YCP to B cells was a direct, saturable and reversible event and required TLR2 and TLR4 involvement. TLR2 and TLR4 defunctionalization by either antibody blocking or allele-specific mutation significantly impaired the B-cell proliferative and IgM responses to YCP. YCP interaction with TLR2 and TLR4 led to the activation of intracellular p38, ERK and JNK, as well as the translocation of transcriptional factor NF-kB into nucleus. Furthermore, specific inhibitors of p38, ERK, JNK and NF-kB could attenuate the ability of YCP to induce B cell proliferation and IgM production. Taken together, this study has indicated for the first time the immunostimulating properties of YCP on B cells through a receptor-mediated mechanism, which involves TLR2 and TLR4 and resultant activation of MAPK and NF-kB signaling pathways, thereby highlighting the role of YCP as an efficacious biological response modifier in oncologic immunotherapy.

 

Click To View

Additional Books


  • Plos One : Epithelial-mesenchymal Transi... (by )
  • Plos One : Human Cytomegalovirus Induces... (by )
  • Plos One : Tv Viewing and Bmi by Race, V... (by )
  • Plos One : Identification and Analysis o... (by )
  • Plos One : Lc-ms, Volume 8 (by )
  • Plos One : Intestinal Parasitic Infectio... (by )
  • Plos One : Autotaxin Signaling Governs P... (by )
  • Plos One : a Targetron System for Gene T... (by )
  • Plos One : Tlm-quant ; an Open-source Pi... (by )
  • Plos One : a Synthetic Form of Frizzled ... (by )
  • Plos One : Omissions and Byproducts Acro... (by )
  • Plos One : Channel Selection Based on Ph... (by )
Scroll Left
Scroll Right

 



Copyright © World Library Foundation. All rights reserved. eBooks from World Library are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.