Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11-12
pubmed:dateCreated
1998-10-22
pubmed:abstractText
Bacterial DNA causes B cell proliferation, immunoglobulin secretion, and Th1-like cytokine secretion, due to unmethylated CpG dinucleotides in particular base contexts (CpG motifs), which are far more common in bacterial DNA than in vertebrate DNA. Synthetic oligodeoxynucleotides (ODN) containing CpG motifs also trigger immune activation, suggesting possible utility as vaccine enhancers. Mice systemically primed with formalin-inactivated influenza virus mixed with CpG ODN, generated virus-specific serum antibodies at titres approximately seven times higher than mice immunized without CpG; the titres were further increased following an identical second injection. To determine whether CpG could be absorbed through mucosae and enhance vaccination responses, mice were immunized intranasally (IN) with the same preparation of virus with or without CpG ODN or Escherichia coli DNA. Following IN immunization, CpG ODN or E. coli DNA promoted increased production of influenza-specific antibodies in serum, saliva and the genital tract, compared with the control groups. These studies indicate that stimulatory CpG ODN are promising new immune enhancers for vaccination applications.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0264-410X
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1216-24
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
CpG DNA, a novel immune enhancer for systemic and mucosal immunization with influenza virus.
pubmed:affiliation
Department of Microbiology, University of Alabama at Birmingham 35294-2170, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't