Linked Life Data

10679096

Source:http://linkedlifedata.com/resource/pubmed/id/10679096

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2000-3-23
pubmed:abstractText
We demonstrated that IL-12 was induced during primary or secondary pulmonary adenoviral infection in wild-type (wt) mice. However, cellular responses were not compromised in the lungs of IL-12-/- mice. The level of IFN-gamma in the lung was similar in wt and IL-12-/- mice during pulmonary viral infection. Upon Ag stimulation in vitro, lymphocytes from draining lymph nodes or spleen of infected IL-12-/- mice released large amounts of IFN-gamma, but not IL-4, which were comparable to those released by wt lymphocytes. Furthermore, a predominantly IgG2a response to adenoviral infection was unimpaired in IL-12-/- mice. These significant anti-adenoviral Th1-type responses in IL-12-/- mice led to an efficient clearance of virus-infected cells in the lung. Whether IL-18 was involved in IL-12-independent anti-adenoviral immune responses was investigated. Abrogation of endogenous IL-18 by an Ab resulted in diminished IFN-gamma release and lymphocytic infiltrate in the lung during adenoviral infection. Nevertheless, the development of lymphocytes of the Th1 phenotype was unimpaired in the absence of both IL-12 and IL-18. In contrast to their intact ability to mount Th1-type responses to viral infection, IL-12-/- mice suffered impaired Th1-type immune responses to pulmonary mycobacterial infection. Our findings suggest that IL-12, although induced, is not required for Th1-type responses to respiratory viral infection, in contrast to mycobacterial infection. IL-18 is required for the optimal release of IFN-gamma in the lung during viral infection, but is not required for the generation of virus-reactive Th1-type lymphocytes. Th1 differentiation during respiratory adenoviral infection may involve molecules different from IL-12 or IL-18.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
164
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2575-84
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10679096-Adenoviridae Infections, pubmed-meshheading:10679096-Adenoviruses, Human, pubmed-meshheading:10679096-Animals, pubmed-meshheading:10679096-Antibodies, Viral, pubmed-meshheading:10679096-Cell Differentiation, pubmed-meshheading:10679096-Chemokine CCL11, pubmed-meshheading:10679096-Chemokines, CC, pubmed-meshheading:10679096-Cytokines, pubmed-meshheading:10679096-Female, pubmed-meshheading:10679096-Gene Expression Regulation, pubmed-meshheading:10679096-Immunophenotyping, pubmed-meshheading:10679096-Interferon-gamma, pubmed-meshheading:10679096-Interleukin-12, pubmed-meshheading:10679096-Interleukin-18, pubmed-meshheading:10679096-Lung, pubmed-meshheading:10679096-Lung Diseases, pubmed-meshheading:10679096-Lymph Nodes, pubmed-meshheading:10679096-Macrophages, Alveolar, pubmed-meshheading:10679096-Male, pubmed-meshheading:10679096-Mice, pubmed-meshheading:10679096-Mice, Inbred C57BL, pubmed-meshheading:10679096-Mice, Knockout, pubmed-meshheading:10679096-Mycobacterium bovis, pubmed-meshheading:10679096-Spleen, pubmed-meshheading:10679096-Th1 Cells, pubmed-meshheading:10679096-Transgenes, pubmed-meshheading:10679096-Tuberculosis, Pulmonary
pubmed:year
2000
pubmed:articleTitle
IL-12-independent Th1-type immune responses to respiratory viral infection: requirement of IL-18 for IFN-gamma release in the lung but not for the differentiation of viral-reactive Th1-type lymphocytes.
pubmed:affiliation
Department of Pathology and Molecular Medicine and Division of Infectious Diseases, Centre for Gene Therapeutics, McMaster University, Hamilton, Ontario, Canada. xingz@fhs.csu.mcmaster.ca
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't