Linked Life Data

17250590

Source:http://linkedlifedata.com/resource/pubmed/id/17250590

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2007-5-17
pubmed:abstractText
Clarifying how an initial protective immune response to tuberculosis may later loose its efficacy is essential to understand tuberculosis pathology and to develop novel vaccines. In mice, a primary vaccination with Ag85B-encoding plasmid DNA (DNA-85B) was protective against Mycobacterium tuberculosis (MTB) infection and associated with Ag85B-specific CD4+ T cells producing IFN-gamma and controlling intramacrophagic MTB growth. Surprisingly, this protection was eliminated by Ag85B protein boosting. Loss of protection was associated with a overwhelming CD4+ T cell proliferation and IFN-gamma production in response to Ag85B protein, despite restraint of Th1 response by CD8+ T cell-dependent mechanisms and activation of CD4+ T cell-dependent IL-10 secretion. Importantly, these Ag85B-responding CD4+ T cells lost the ability to produce IFN-gamma and control MTB intramacrophagic growth in coculture with MTB-infected macrophages, suggesting that the protein-dependent expansion of non-protective CD4+ T cells determined dilution or loss of the protective Ag85B-specific CD4+ induced by DNA-85B vaccination. These data emphasize the need of exerting some caution in adopting aggressive DNA-priming, protein-booster schedules for MTB vaccines. They also suggest that Ag85B protein secreted during MTB infection could be involved in the instability of protective anti-tuberculosis immune response, and actually concur to disease progression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1462-5814
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1455-65
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:17250590-Acyltransferases, pubmed-meshheading:17250590-Animals, pubmed-meshheading:17250590-Antigens, Bacterial, pubmed-meshheading:17250590-Bacterial Proteins, pubmed-meshheading:17250590-CD4-Positive T-Lymphocytes, pubmed-meshheading:17250590-Female, pubmed-meshheading:17250590-Interferon-gamma, pubmed-meshheading:17250590-Macrophages, pubmed-meshheading:17250590-Mice, pubmed-meshheading:17250590-Mice, Inbred C57BL, pubmed-meshheading:17250590-Mycobacterium tuberculosis, pubmed-meshheading:17250590-Specific Pathogen-Free Organisms, pubmed-meshheading:17250590-Spleen, pubmed-meshheading:17250590-T-Lymphocyte Subsets, pubmed-meshheading:17250590-T-Lymphocytes, Helper-Inducer, pubmed-meshheading:17250590-Tuberculosis, pubmed-meshheading:17250590-Tuberculosis Vaccines, pubmed-meshheading:17250590-Vaccines, DNA
pubmed:year
2007
pubmed:articleTitle
The Ag85B protein of Mycobacterium tuberculosis may turn a protective immune response induced by Ag85B-DNA vaccine into a potent but non-protective Th1 immune response in mice.
pubmed:affiliation
Department of Infectious, Parasitic and Immune-mediated Diseases, Istituto Superiore di Sanità, Rome, Italy. c.palma@iss.it
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't