The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
A Protease-Activated Pathway Underlying Th Cell Type 2 Activation and Allergic Lung Disease
Abstract
The respiratory allergens that induce experimental Th cell type 2-dependent allergic lung inflammation may be grouped into two functional classes. One class of allergens, in this study termed type I, requires priming with adjuvants remote from the lung to overcome airway tolerogenic mechanisms that ordinarily preclude allergic responses to inhaled Ags. In contrast, the other, or type II, allergen class requires neither remote priming nor additional adjuvants to overcome airway tolerance and elicit robust allergic lung disease. In this study, we show in an experimental model that diverse type II allergens share in common proteolytic activity that is both necessary and sufficient for overcoming airway tolerance and induction of pulmonary allergic disease. Inactivated protease and protease-free Ag fragments showed no allergenic potency, demonstrating that only active protease acting on endogenous substrates was essential. Furthermore, induction of airway tolerance could be aborted and allergic lung disease established by simply adding purified protease to a type I allergen. Thus, exogenous proteases are common to type II allergens and may be generally required to overcome the innate resistance of the airway to Th cell type 2 activation and allergic inflammation, raising concern for their potential contribution to diseases such as asthma.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Jonjić, S., Mutter, W., Weiland, F., Reddehase, M. J., & Koszinowski, U. H. (1989) · The Journal of experimental medicine · doi:10.1084/jem.169.4.1199 · Cited by 2,105
Requirement for IL-13 Independently of IL-4 in Experimental Asthma
Grünig, G., Warnock, M., Wakil, A. E., Venkayya, R., Brombacher, F., Rennick, D. M., Sheppard, D., Mohrs, M., Donaldson, D. D., Locksley, R. M., et al. (1998) · Science · doi:10.1126/science.282.5397.2261 · Cited by 1,849
Self-citationToll-like receptors control activation of adaptive immune responses
Schnare, M., Barton, G. M., Holt, A. C., Takeda, K., Akira, S., & Medzhitov, R. (2001) · Nature Immunology · doi:10.1038/ni712 · Cited by 1,365
Regulation of antibody isotype secretion by subsets of antigen-specific helper T cells
Stevens, T. L., Bossie, A., Sanders, V. M., Fernandez-Botran, R., Coffman, R. L., Mosmann, T. R., & Vitetta, E. S. (1988) · Nature · doi:10.1038/334255a0 · Cited by 933
Der p 1 facilitates transepithelial allergen delivery by disruption of tight junctions
Wan, H., Winton, H. L., Soeller, C., Tovey, E. R., Gruenert, D. C., Thompson, P. J., Stewart, G. A., Taylor, G. W., Garrod, D. R., Cannell, M. B., et al. (1999) · Journal of Clinical Investigation · doi:10.1172/jci5844 · Cited by 775
IFN- gamma regulates the isotypes of Ig secreted during in vivo humoral immune responses.
Finkelman, F. D., Katona, I. M., Mosmann, T. R., & Coffman, R. L. (1988) · The Journal of Immunology · doi:10.4049/jimmunol.140.4.1022 · Cited by 723
Corry, D. B., Folkesson, H. G., Warnock, M. L., Erle, D. J., Matthay, M. A., Wiener-Kronish, J. P., & Locksley, R. M. (1996) · The Journal of experimental medicine · doi:10.1084/jem.183.1.109 · Cited by 722
Self-citationIL-4 is required to generate and sustain in vivo IgE responses.
Finkelman, F. D., Katona, I. M., Urban, J. F., Holmes, J., Ohara, J., Tung, A. S., Sample, J. V., & Paul, W. E. (1988) · The Journal of Immunology · doi:10.4049/jimmunol.141.7.2335 · Cited by 668
Dust mites: Immunology, allergic disease, and environmental control
Platts-Mills, T. A. E., & Chapman, M. D. (1987) · Journal of Allergy and Clinical Immunology · doi:10.1016/s0091-6749(87)80261-0 · Cited by 468
Attenuation of allergic airway inflammation in IL‐4 deficient mice
BRUSSELLE, G. G., KIPS, J. C., TAVERNIER, J. H., VAN DER HEYDEN, J. G., CUVELIER, C. A., PAUWELS, R. A., & BLUETHMANN, H. (1994) · Clinical & Experimental Allergy · doi:10.1111/j.1365-2222.1994.tb00920.x · Cited by 431
Cited by
A mechanism for the initiation of allergen-induced T helper type 2 responses
Sokol, C. L., Barton, G. M., Farr, A. G., & Medzhitov, R. (2008) · Nature Immunology · doi:10.1038/ni1558 · Cited by 961
The link between fungi and severe asthma: A summary of the evidence
Denning, D. W., O'Driscoll, B. R., Hogaboam, C. M., Bowyer, P., & Niven, R. M. (2006) · European Respiratory Journal · doi:10.1183/09031936.06.00074705 · Cited by 824
de Heer, H. J., Hammad, H., Soullié, T., Hijdra, D., Vos, N., Willart, M. A. M., Hoogsteden, H. C., & Lambrecht, B. N. (2004) · The Journal of Experimental Medicine · doi:10.1084/jem.20040035 · Cited by 785
Interleukin‐13 in asthma pathogenesis
Wills‐Karp, M. (2004) · Immunological Reviews · doi:10.1111/j.0105-2896.2004.00215.x · Cited by 683
Dendritic cells and epithelial cells: linking innate and adaptive immunity in asthma
Hammad, H., & Lambrecht, B. N. (2008) · Nature Reviews Immunology · doi:10.1038/nri2275 · Cited by 666
Metadata
- Authors
- Kheradmand, F., Kiss, A., Xu, J., Lee, S.-H., Kolattukudy, P. E., & Corry, D. B.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-11
- Volume
- 169
- Issue
- 10
- Pages
- 5904-5911
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2154719091
- Cited by
- 305
- References
- 61
- FWCI
- 4.78
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: A Protease-Activated Pathway Underlying Th Cell Type 2 Activation and Allergic Lung Disease. https://app.cochat.ai/papers/10.4049/jimmunol.169.10.5904
- The paper
- Kheradmand, F., Kiss, A., Xu, J., Lee, S.-H., Kolattukudy, P. E., & Corry, D. B. (2002). A Protease-Activated Pathway Underlying Th Cell Type 2 Activation and Allergic Lung Disease. The Journal of Immunology. https://doi.org/10.4049/jimmunol.169.10.5904
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.