The DOI matches its Crossref record; 102 of the 102 references it cites were found in a registry or an index.
IMMUNOLOGIC BASIS OF ANTIGEN-INDUCED AIRWAY HYPERRESPONSIVENESS
Abstract
▪ Abstract The incidence, morbidity, and mortality of asthma has increased worldwide over the last two decades. Asthma is a complex inflammatory disease of the lung characterized by variable airflow obstruction, airway hyperresponsiveness (AHR), and airway inflammation. The inflammatory response in the asthmatic lung is characterized by infiltration of the airway wall with mast cells, lymphocytes, and eosinophils. Although asthma is multifactorial in origin, the inflammatory process in the most common form of the disease (extrinsic asthma) is believed to be a result of inappropriate immune responses to common aero-allergens in genetically susceptible individuals. As such, it has been hypothesized that CD4+T cells that produce a Th2 pattern of cytokines play a pivotal role in the pathogenesis of this disease. Through the release of cytokines such as IL-4, IL-13, and IL-5, these cells orchestrate the recruitment and activation of the primary effector cells of the allergic response, the mast cell and the eosinophil. Activation of these cells results in the release of a plethora of inflammatory mediators that individually or in concert induce changes in airway wall geometry and produce the symptoms of the disease. The aim of this review is to discuss our current understanding of the pathophysiologic mechanisms by which Th2 cytokines induce airway disease, and the factors that predispose to the generation of these pathogenic cells in response to inhalation of ubiquitous aero-allergens. Elucidation of the exact immunological basis for allergic asthma may yield immunotherapeutic strategies to reverse the development of pathogenic Th2-mediated immune responses and reduce the morbidity and mortality associated with this disease.
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
Mosmann, T. R., Cherwinski, H., Bond, M. W., Giedlin, M. A., & Coffman, R. L. (1986) · The Journal of Immunology · doi:10.4049/jimmunol.136.7.2348 · Cited by 7,506
Development of T H 1 CD4 + T Cells Through IL-12 Produced by Listeria -Induced Macrophages
Hsieh, C.-S., Macatonia, S. E., Tripp, C. S., Wolf, S. F., O'Garra, A., & Murphy, K. M. (1993) · Science · doi:10.1126/science.8097338 · Cited by 3,134
Predominant TH2-like Bronchoalveolar T-Lymphocyte Population in Atopic Asthma
Robinson, D. S., Hamid, Q., Ying, S., Tsicopoulos, A., Barkans, J., Bentley, A. M., Corrigan, C., Durham, S. R., & Kay, A. B. (1992) · New England Journal of Medicine · doi:10.1056/nejm199201303260504 · Cited by 2,768
Eosinophilic Inflammation in Asthma
Bousquet, J., Chanez, P., Lacoste, J. Y., Barnéon, G., Ghavanian, N., Enander, I., Venge, P., Ahlstedt, S., Simony-Lafontaine, J., Godard, P., et al. (1990) · New England Journal of Medicine · doi:10.1056/nejm199010113231505 · Cited by 2,499
Bronchial reactivity to inhaled histamine: a method and clinical survey
COCKCROFT, D. W., KILLIAN, D. N., MELLON, J. J. A., & HARGREAVE, F. E. (1977) · Clinical & Experimental Allergy · doi:10.1111/j.1365-2222.1977.tb01448.x · Cited by 1,840
Metcalfe, D. D., Baram, D., & Mekori, Y. A. (1997) · Physiological Reviews · doi:10.1152/physrev.1997.77.4.1033 · Cited by 1,724
Dendritic cells produce IL-12 and direct the development of Th1 cells from naive CD4+ T cells.
Macatonia, S. E., Hosken, N. A., Litton, M., Vieira, P., Hsieh, C. S., Culpepper, J. A., Wysocka, M., Trinchieri, G., Murphy, K. M., & O'Garra, A. (1995) · The Journal of Immunology · doi:10.4049/jimmunol.154.10.5071 · Cited by 1,524
Foster, P. S., Hogan, S. P., Ramsay, A. J., Matthaei, K. I., & Young, I. G. (1996) · The Journal of experimental medicine · doi:10.1084/jem.183.1.195 · Cited by 1,370
The Inverse Association Between Tuberculin Responses and Atopic Disorder
Shirakawa, T., Enomoto, T., Shimazu, S.-I., & Hopkin, J. M. (1997) · Science · doi:10.1126/science.275.5296.77 · Cited by 1,287
Cellular Events in the Bronchi in Mild Asthma and after Bronchial Provocation
Beasley, R., Roche, W. R., Roberts, J. A., & Holgate, S. T. (1989) · American Review of Respiratory Disease · doi:10.1164/ajrccm/139.3.806 · Cited by 1,128
Cited by
The Endocannabinoid System as an Emerging Target of Pharmacotherapy
Pacher, P., Bátkai, S., & Kunos, G. (2006) · Pharmacological Reviews · doi:10.1124/pr.58.3.2 · Cited by 2,077
The development of allergic inflammation
Galli, S. J., Tsai, M., & Piliponsky, A. M. (2008) · Nature · doi:10.1038/nature07204 · Cited by 1,839
Interleukin‐13 in asthma pathogenesis
Wills‐Karp, M. (2004) · Immunological Reviews · doi:10.1111/j.0105-2896.2004.00215.x · Cited by 683
Self-citationBullens, D. M., Truyen, E., Coteur, L., Dilissen, E., Hellings, P. W., Dupont, L. J., & Ceuppens, J. L. (2006) · Respiratory Research · doi:10.1186/1465-9921-7-135 · Cited by 587
Disruption of Nrf2 enhances susceptibility to severe airway inflammation and asthma in mice
Rangasamy, T., Guo, J., Mitzner, W. A., Roman, J., Singh, A., Fryer, A. D., Yamamoto, M., Kensler, T. W., Tuder, R. M., Georas, S. N., et al. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20050538 · Cited by 580
Metadata
- Authors
- Wills-Karp, M.
- Venue
- Annual Review of Immunology
- Publisher
- Annual Reviews
- Published
- 1999-04
- Volume
- 17
- Issue
- 1
- Pages
- 255-281
- ISSN
- 0732-0582 (ISSN-L)
- 1545-3278
- OpenAlex
- W2136651927
- Cited by
- 1,020
- References
- 102
- FWCI
- 7.68
- 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: IMMUNOLOGIC BASIS OF ANTIGEN-INDUCED AIRWAY HYPERRESPONSIVENESS. https://app.cochat.ai/papers/10.1146/annurev.immunol.17.1.255
- The paper
- Wills-Karp, M. (1999). IMMUNOLOGIC BASIS OF ANTIGEN-INDUCED AIRWAY HYPERRESPONSIVENESS. Annual Review of Immunology. https://doi.org/10.1146/annurev.immunol.17.1.255
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.
