| pubmed-article:9670970 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9670970 | lifeskim:mentions | umls-concept:C0123759 | lld:lifeskim |
| pubmed-article:9670970 | lifeskim:mentions | umls-concept:C0458827 | lld:lifeskim |
| pubmed-article:9670970 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:9670970 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:9670970 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:9670970 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
| pubmed-article:9670970 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:9670970 | pubmed:dateCreated | 1998-7-30 | lld:pubmed |
| pubmed-article:9670970 | 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. | lld:pubmed |
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| pubmed-article:9670970 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9670970 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9670970 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:9670970 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9670970 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:9670970 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:9670970 | pubmed:author | pubmed-author:WysockaMM | lld:pubmed |
| pubmed-article:9670970 | pubmed:author | pubmed-author:TrinchieriGG | lld:pubmed |
| pubmed-article:9670970 | pubmed:author | pubmed-author:Wills-KarpMM | lld:pubmed |
| pubmed-article:9670970 | pubmed:author | pubmed-author:Keane-MyersAA | lld:pubmed |
| pubmed-article:9670970 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9670970 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:9670970 | pubmed:volume | 161 | lld:pubmed |
| pubmed-article:9670970 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9670970 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9670970 | pubmed:pagination | 919-26 | lld:pubmed |
| pubmed-article:9670970 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:9670970 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9670970 | pubmed:articleTitle | Resistance to antigen-induced airway hyperresponsiveness requires endogenous production of IL-12. | lld:pubmed |
| pubmed-article:9670970 | pubmed:affiliation | Department of Environmental Health Sciences, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, MD 21205, USA. | lld:pubmed |
| pubmed-article:9670970 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9670970 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9670970 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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