Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2008-7-10
pubmed:abstractText
SUMMARY: The innate immune system is a critical element of protection from invading pathogens. The specific receptors that recognize various components of the pathogens trigger signals that result in the production of proinflammatory cytokines as well as the activation of antigen-presenting cells, which activate the adaptive immune system. The discovery of the Toll-like receptors (TLRs) as important components of pathogen recognition has brought new understanding of the key signaling molecules involves in innate immune activation. Interestingly, it appears that most TLRs can recognize self-ligands as well and that mechanisms are required to discriminate between self and non-self ligands. One of these mechanisms is the expression of all the nucleic acid-specific TLR in endosomal compartments and not on the cell surface. Inappropriate activation of TLRs by self-components can result in sterile inflammation or autoimmunity. For example, TLR7 and TLR9 activation by endogenous RNA and DNA, transported to the endosomes in the form of immune complexes or non-covalently associated with cationic peptides, could be an important mechanism involved in promoting diseases such as systemic lupus erythematosus and psoriasis. In this review, we discuss the rationale for self-recognition by TLR7 and TLR9 as an important part of the development of lupus and other autoimmune diseases. We describe novel inhibitors of these receptors and provide evidence to support their use as novel therapeutic agents for autoimmunity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1600-065X
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
223
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
271-83
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Development of TLR inhibitors for the treatment of autoimmune diseases.
pubmed:affiliation
Dynavax Technologies Corporation, Berkeley, CA 94710, USA. fbarrat@dynavax.com
pubmed:publicationType
Journal Article, Review