Source:http://linkedlifedata.com/resource/pubmed/id/17000223
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
2006-9-26
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pubmed:abstractText |
A significant amount of data generated over the last few years supports the contention that Toll-like receptor (TLR) 9-based immunotherapy is effective in the prevention and treatment of animal models of allergic disorders. We will review here our experience with two distinct therapeutic strategies: TLR9-based immunomodulation and TLR9-based vaccination. Immunomodulation of allergic inflammation by TLR9 ligand (TLR9-L) is transient. It prevents both the early and late phases of the allergic reaction in experimental models of allergic asthma, rhinitis, and conjunctivitis. It also reverses ongoing allergic inflammation. Indoleamine 2.3-dioxygenase, the rate-limiting enzyme of tryptophan, is induced by TLR9-L and mediates, in part, these anti-inflammatory effects. TLR9-based immunomodulation is independent of allergens and, therefore, has a potential therapeutic advantage in a broad spectrum of allergic patients. On the other hand, TLR9-based vaccination therapy is an allergen-specific mode of immunotherapy, which provides long-term inhibition of allergen-specific hypersensitivities. Current clinical trials with TLR9-based immunotherapy demonstrate high immunogenic and therapeutic efficacy, as well as improved safety when compared with conventional allergen desensitization. Thus, if proven efficient, therapeutic strategies with TLR9-L may revolutionize the current treatment of allergic diseases.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1555-7162
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
119
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
897.e1-6
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading | |
pubmed:year |
2006
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pubmed:articleTitle |
TLR9-based immunotherapy for allergic disease.
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pubmed:affiliation |
Department of Medicine, University of California San Diego, La Jolla CA, 92093, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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