DOI: 10.4049/jimmunol.161.2.919. Resistance to Antigen-Induced Airway Hyperresponsiveness Requires Endogenous Production of IL-12

Resistance to Antigen-Induced Airway Hyperresponsiveness Requires Endogenous Production of IL-12

10.4049/jimmunol.161.2.919

Crossref journal-article

Oxford University Press (OUP)

The Journal of Immunology (286)

Abstract

AbstractWe 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-γ 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-γ. 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.

Bibliography

Keane-Myers, A., Wysocka, M., Trinchieri, G., & Wills-Karp, M. (1998). Resistance to Antigen-Induced Airway Hyperresponsiveness Requires Endogenous Production of IL-12. The Journal of Immunology, 161(2), 919â926.

Authors 4

Andrea Keane-Myers (first)
Maria Wysocka (additional)
Giorgio Trinchieri (additional)
Marsha Wills-Karp (additional)

References 45 Referenced 49

Dates

Type	When
Created	2 years, 8 months ago (Dec. 31, 2022, 9:20 a.m.)
Deposited	8 months ago (Jan. 2, 2025, 11:31 a.m.)
Indexed	3 months, 1 week ago (May 20, 2025, 2:04 p.m.)
Issued	27 years, 1 month ago (July 15, 1998)
Published	27 years, 1 month ago (July 15, 1998)
Published Print	27 years, 1 month ago (July 15, 1998)

Funders 0

None

BibTeX

@article{Keane_Myers_1998, title={Resistance to Antigen-Induced Airway Hyperresponsiveness Requires Endogenous Production of IL-12}, volume={161}, ISSN={1550-6606}, url={http://dx.doi.org/10.4049/jimmunol.161.2.919}, DOI={10.4049/jimmunol.161.2.919}, number={2}, journal={The Journal of Immunology}, publisher={Oxford University Press (OUP)}, author={Keane-Myers, Andrea and Wysocka, Maria and Trinchieri, Giorgio and Wills-Karp, Marsha}, year={1998}, month=jul, pages={919–926} }

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  "abstract": "<jats:title>Abstract</jats:title><jats:p>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-\u03b3 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-\u03b3. 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.</jats:p>",
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