The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.
A sthma : Mechanisms of Disease Persistence and Progression
Abstract
▪ Abstract When asthma is diagnosed, eosinophilic inflammation and airway remodeling are established in the bronchial airways and can no longer be separated as cause and effect because both processes contribute to persistence and progression of disease, despite anti-inflammatory therapy. Th2 cells are continually active in the airways, even when disease is quiescent. IL-13 is the key effector cytokine in asthma and stimulates airway fibrosis through the action of matrix metalloproteinases on TGF-β and promotes epithelial damage, mucus production, and eosinophilia. The production of IL-13 and other Th2 cytokines by non-T cells augments the inflammatory response. Inflammation is amplified by local responses of the epithelium, smooth muscle, and fibroblasts through the production of chemokines, cytokines, and proteases. Injured cells produce adenosine that enhances IL-13 production. We review human and animal data detailing the cellular and molecular interactions in established allergic asthma that promote persistent disease, amplify inflammation, and, in turn, cause disease progression.
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
Lee, C. G., Homer, R. J., Zhu, Z., Lanone, S., Wang, X., Koteliansky, V., Shipley, J. M., Gotwals, P., Noble, P., Chen, Q., et al. (2001) · The Journal of Experimental Medicine · doi:10.1084/jem.194.6.809 · Cited by 940
Self-citationFerrick, D. A., Schrenzel, M. D., Mulvania, T., Hsieh, B., Ferlin, W. G., & Lepper, H. (1995) · Nature · doi:10.1038/373255a0 · Cited by 662
Temann, U.-A., Geba, G. P., Rankin, J. A., & Flavell, R. A. (1998) · The Journal of Experimental Medicine · doi:10.1084/jem.188.7.1307 · Cited by 452
New insights into the pathogenesis of asthma
Elias, J. A., Lee, C. G., Zheng, T., Ma, B., Homer, R. J., & Zhu, Z. (2003) · Journal of Clinical Investigation · doi:10.1172/jci17748 · Cited by 407
Self-citationAirway Epithelial Cells Release MIP-3α/CCL20 in Response to Cytokines and Ambient Particulate Matter
Reibman, J., Hsu, Y., Chen, L. C., Bleck, B., & Gordon, T. (2003) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2002-0095oc · Cited by 262
Pulmonary overexpression of IL-9 induces Th2 cytokine expression, leading to immune pathology
Temann, U.-A., Ray, P., & Flavell, R. A. (2002) · Journal of Clinical Investigation · doi:10.1172/jci0213696 · Cited by 201
Cited by
The development of allergic inflammation
Galli, S. J., Tsai, M., & Piliponsky, A. M. (2008) · Nature · doi:10.1038/nature07204 · Cited by 1,839
Woodruff, P. G., Boushey, H. A., Dolganov, G. M., Barker, C. S., Yang, Y. H., Donnelly, S., Ellwanger, A., Sidhu, S. S., Dao-Pick, T. P., Pantoja, C., et al. (2007) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0707413104 · Cited by 828
Halim, T. Y. F., Krauß, R. H., Sun, A. C., & Takei, F. (2012) · Immunity · doi:10.1016/j.immuni.2011.12.020 · Cited by 804
MHC class II–dependent basophil–CD4+ T cell interactions promote TH2 cytokine–dependent immunity
Perrigoue, J. G., Saenz, S. A., Siracusa, M. C., Allenspach, E. J., Taylor, B. C., Giacomin, P. R., Nair, M. G., Du, Y., Zaph, C., van Rooijen, N., et al. (2009) · Nature Immunology · doi:10.1038/ni.1740 · Cited by 601
Wang, Y.-H., Voo, K. S., Liu, B., Chen, C.-Y., Uygungil, B., Spoede, W., Bernstein, J. A., Huston, D. P., & Liu, Y.-J. (2010) · Journal of Experimental Medicine · doi:10.1084/jem.20101376 · Cited by 431
Metadata
- Authors
- Cohn, L., Elias, J. A., & Chupp, G. L.
- Venue
- Annual Review of Immunology
- Publisher
- Annual Reviews
- Published
- 2004-04-01
- Volume
- 22
- Issue
- 1
- Pages
- 789-815
- ISSN
- 0732-0582 (ISSN-L)
- 1545-3278
- OpenAlex
- W2164692566
- Cited by
- 812
- References
- 6
- FWCI
- 4.34
- 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 sthma : Mechanisms of Disease Persistence and Progression. https://app.cochat.ai/papers/10.1146/annurev.immunol.22.012703.104716
- The paper
- Cohn, L., Elias, J. A., & Chupp, G. L. (2004). A sthma : Mechanisms of Disease Persistence and Progression. Annual Review of Immunology. https://doi.org/10.1146/annurev.immunol.22.012703.104716
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.