Linked Life Data

17197239

Source:http://linkedlifedata.com/resource/pubmed/id/17197239

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-2-5
pubmed:abstractText
Toll-like receptor (TLR) activation by pathogens can induce the activation of diverse cell populations of the immune system and, therefore, can initiate or augment protective T-helper 1 immune responses. However, on a susceptible genetic background, TLR stimulation can also induce autoimmunity. The relative contribution of either microbe-derived or endogenous antigens, such as single-stranded RNA and unmethylated DNA, to TLR stimulation and the development of specific autoimmune diseases are still debated. Here, we review the different possibilities. Furthermore, tolerance induction by TLRs, which originally had been postulated to be protective by limiting excessive inflammation and, thus, preventing septic shock, has come into focus as a mechanism to control autoimmunity by inhibiting dendritic-cell maturation. In some murine models of systemic lupus erythematosus, TLR9 deficiency results in a shift from anti-nucleosome to TLR7-dependent anti-ribonucleoprotein IgG2a and IgG2b autoantibodies, and enhanced disease progression and mortality. Thus, not only can TLR signalling induce autoimmunity, but TLR(9) stimulation might also regulate tolerance.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1471-4906
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
74-9
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Opposing effects of Toll-like receptor stimulation induce autoimmunity or tolerance.
pubmed:affiliation
Laboratory of Tolerance and Autoimmunity, German Arthritis Research Center (DRFZ), D-10117 Berlin, Germany. ehlers@drfz.de
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't