Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-8-9
pubmed:abstractText
In the last decade, substantial progress has been made in understanding the molecular mechanisms involved in initial host responses to viral infections, and how viral recognition leads to the innate responses that ultimately shape the adaptive immune response. Viruses, including herpes simplex virus (HSV) types 1 and 2, trigger toll-like receptors (TLRs) that elicit cytokine and chemokine production. In turn, this can create local resistance and modulate T- and B-cell-mediated immunity. TLR activation by HSV-produced molecules (or other synthetic agonists) leads to the remodelling of draining lymph nodes. This enhances the screening of naive T-cells, from which antigen-specific lymphocytes can be selected and expanded. The innate response thereby serves to direct a timely and effective acquired immune response, through the initial TLR recognition of viral pathogen-associated molecular patterns that can limit or possibly exacerbate viral pathogenesis. Recently, these findings have been exploited by strategies that utilize synthetic TLR agonists as prophylactic or therapeutic devices. Such devices prime innate immune responses, enhancing host resistance to viral infections, including experimental HSV infections.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0969-7667
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
37-41
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Toll-like receptors, innate immunity and HSV pathogenesis.
pubmed:affiliation
Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555-0436, USA.
pubmed:publicationType
Journal Article, Review