Abstract:
:Toll-like receptors (TLRs) are important initiators in innate immune responses against pathogenic microbes such as viruses, intracellular bacteria or parasites. Although the innate immune system is designed to fight infectious pathogens, excessive activation of TLR signaling may lead to unwarranted inflammation with hazardous outcomes. Mechanisms of restraining excessive inflammation and controlling homeostasis for innate immunity are the focus of intense study. Here we showed that LRRC33, a novel member of leucine-rich repeat (LRR) protein family, plays a critical role in desensitizing TLR signaling. LRRC33 is TLR homolog that contains 17 putative LRRs in the extracellular region but lacks a cytoplasmic Toll/IL-1 receptor (TIR) domain. Expression of LRRC33 appears to be ubiquitous with high level of expression found in bone marrow, thymus, liver, lung, intestine and spleen. The LRRs of LRRC33 is required for the interaction with TLR and its inhibitory effect on NF-κB and AP-1 activation as well as cytokine production. Our study sheds new insight into the TLR signaling and inflammatory response in development and human diseases.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Liu J,Zhang Z,Chai L,Che Y,Min S,Yang Rdoi
10.1016/j.bbrc.2013.03.071subject
Has Abstractpub_date
2013-04-26 00:00:00pages
28-34issue
1eissn
0006-291Xissn
1090-2104pii
S0006-291X(13)00525-1journal_volume
434pub_type
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