Please use this identifier to cite or link to this item:
|Title:||MHC class II-associated invariant chain (Ii) modulates dendritic cells-derived microvesicles (DCMV)-mediated activation of microglia||Authors:||Teo, B.H.D.
|Issue Date:||1-Oct-2010||Citation:||Teo, B.H.D., Wong, S.H. (2010-10-01). MHC class II-associated invariant chain (Ii) modulates dendritic cells-derived microvesicles (DCMV)-mediated activation of microglia. Biochemical and Biophysical Research Communications 400 (4) : 673-678. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbrc.2010.08.126||Abstract:||Dendritic cells (DC) - the sentinels of the immune system - play an important role in the maintenance of tolerance and induction of immunity. However, in autoimmune diseases, DC initiate the diseases by presenting self antigens to autoreactive T cells, causing the immune system to mount a response against the body. An example is multiple sclerosis (MS) and its corresponding animal model, experimental autoimmune encephalomyelitis (EAE). During inflammation of the central nervous system (CNS), DC are recruited to activate autoreactive T cells. Microglia - resident mononuclear phagocytes of the brain - also play a role in the pathogenesis of the disease. In this study, we demonstrated that microvesicles derived from DC (DCMV) induced the activation of NF-κB in microglia. Furthermore, MHC class II-associated invariant chain (Ii), also known as CD74, was specifically recruited to DCMV and interestingly, was able to enhance the DCMV-mediated activation of NF-κB in microglia. Thus, this study emphasizes the role of microvesicles and Ii in the communication between DC and microglia. © 2010 Elsevier Inc.||Source Title:||Biochemical and Biophysical Research Communications||URI:||http://scholarbank.nus.edu.sg/handle/10635/109460||ISSN:||0006291X||DOI:||10.1016/j.bbrc.2010.08.126|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Dec 6, 2019
WEB OF SCIENCETM
checked on Nov 28, 2019
checked on Nov 29, 2019
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.