Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1998-7-30
|
| pubmed:abstractText |
We have demonstrated previously that susceptibility of murine strains to the development of allergic airway responses is associated with a type 2 cytokine pattern. In the present study, we examine the in vivo role of IL-12 in the immune response to allergen exposure in susceptible (A/J) and resistant (C3H/HeJ, C3H) strains of mice. OVA sensitization and challenge induced significant increases in airway reactivity in A/J mice as compared with their PBS-challenged controls, while no increases in airway reactivity were observed in OVA-challenged C3H mice. OVA exposure of A/J mice resulted in marked increases in the Th2 cytokines, IL-4 and IL-10, in the bronchoalveolar lavage fluid, whereas increases in IFN-gamma were observed in C3H mice. Strikingly, anti-IL-12 mAb (1 mg/mouse) treatment resulted in threefold increases in airway reactivity in OVA-challenged resistant C3H mice, concomitant with significant increases in bronchoalveolar lavage levels of Th2 cytokines and decreases in IFN-gamma. IL-12 depletion of C3H mice also suppressed OVA-specific serum IgG2a levels and increased both serum OVA-specific IgG1 and IgE levels. Blockade of endogenous IL-12 levels in susceptible A/J mice resulted in further augmentation of type 2 immune responses. These results demonstrate that endogenous production of IL-12 is essential for resistance to Ag-induced airway hyperresponsiveness, and furthermore, that dysregulation of IL-12 production may lead to the development of deleterious type 2 immune responses to inhaled allergens.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, T-Lymphocyte,
http://linkedlifedata.com/resource/pubmed/chemical/Immune Sera,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin E,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-12,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
|
| pubmed:volume |
161
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
919-26
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:9670970-Animals,
pubmed-meshheading:9670970-Antibodies, Monoclonal,
pubmed-meshheading:9670970-Bronchial Hyperreactivity,
pubmed-meshheading:9670970-Cytokines,
pubmed-meshheading:9670970-Disease Susceptibility,
pubmed-meshheading:9670970-Epitopes, T-Lymphocyte,
pubmed-meshheading:9670970-Immune Sera,
pubmed-meshheading:9670970-Immunity, Innate,
pubmed-meshheading:9670970-Immunoglobulin E,
pubmed-meshheading:9670970-Immunoglobulin G,
pubmed-meshheading:9670970-Injections, Intraperitoneal,
pubmed-meshheading:9670970-Interleukin-12,
pubmed-meshheading:9670970-Lung,
pubmed-meshheading:9670970-Male,
pubmed-meshheading:9670970-Mice,
pubmed-meshheading:9670970-Mice, Inbred A,
pubmed-meshheading:9670970-Mice, Inbred C3H,
pubmed-meshheading:9670970-Ovalbumin,
pubmed-meshheading:9670970-Th2 Cells
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Resistance to antigen-induced airway hyperresponsiveness requires endogenous production of IL-12.
|
| pubmed:affiliation |
Department of Environmental Health Sciences, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, MD 21205, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|