The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
Intrinsic Defect in T Cell Production of Interleukin (IL)-13 in the Absence of Both IL-5 and Eotaxin Precludes the Development of Eosinophilia and Airways Hyperreactivity in Experimental Asthma
Open accessAbstract
Interleukin (IL)-5 and IL-13 are thought to play key roles in the pathogenesis of asthma. Although both cytokines use eotaxin to regulate eosinophilia, IL-13 is thought to operate a separate pathway to IL-5 to induce airways hyperreactivity (AHR) in the allergic lung. However, identification of the key pathway(s) used by IL-5 and IL-13 in the disease process is confounded by the failure of anti–IL-5 or anti–IL-13 treatments to completely inhibit the accumulation of eosinophils in lung tissue. By using mice deficient in both IL-5 and eotaxin (IL-5/eotaxin−/−) we have abolished tissue eosinophilia and the induction of AHR in the allergic lung. Notably, in mice deficient in IL-5/eotaxin the ability of CD4+ T helper cell (Th)2 lymphocytes to produce IL-13, a critical regulator of airways smooth muscle constriction and obstruction, was significantly impaired. Moreover, the transfer of eosinophils to IL-5/eotaxin−/− mice overcame the intrinsic defect in T cell IL-13 production. Thus, factors produced by eosinophils may either directly or indirectly modulate the production of IL-13 during Th2 cell development. Our data show that IL-5 and eotaxin intrinsically modulate IL-13 production from Th2 cells and that these signaling systems are not necessarily independent effector pathways and may also be integrated to regulate aspects of allergic disease.
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Interleukin-13: Central Mediator of Allergic Asthma
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Self-citationInterleukin-18 Regulates Both Th1 and Th2 Responses
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Cited by
Cellular and molecular mechanisms of fibrosis
Wynn, T. (2008) · The Journal of Pathology · doi:10.1002/path.2277 · Cited by 4,495
Chemokines and Chemokine Receptors: Positioning Cells for Host Defense and Immunity
Griffith, J. W., Sokol, C. L., & Luster, A. D. (2014) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032713-120145 · Cited by 2,059
Fibrotic disease and the TH1/TH2 paradigm
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Self-citationEosinophils: changing perspectives in health and disease
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Metadata
- Authors
- Mattes, J., Yang, M., Mahalingam, S., Kuehr, J., Webb, D. C., Simson, L., Hogan, S. P., Koskinen, A., McKenzie, A. N. J., Dent, L. A., Rothenberg, M. E., Matthaei, K. I., Young, I. G., & Foster, P. S.
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2002-06-03
- Volume
- 195
- Issue
- 11
- Pages
- 1433-1444
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- OpenAlex
- W2157340183
- Cited by
- 264
- References
- 51
- FWCI
- 13.41
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Intrinsic Defect in T Cell Production of Interleukin (IL)-13 in the Absence of Both IL-5 and Eotaxin Precludes the Development of Eosinophilia and Airways Hyperreactivity in Experimental Asthma. https://app.cochat.ai/papers/10.1084/jem.20020009
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- Mattes, J., Yang, M., Mahalingam, S., Kuehr, J., Webb, D. C., Simson, L., Hogan, S. P., Koskinen, A., McKenzie, A. N. J., Dent, L. A., Rothenberg, M. E., Matthaei, K. I., Young, I. G., & Foster, P. S. (2002). Intrinsic Defect in T Cell Production of Interleukin (IL)-13 in the Absence of Both IL-5 and Eotaxin Precludes the Development of Eosinophilia and Airways Hyperreactivity in Experimental Asthma. The Journal of Experimental Medicine. https://doi.org/10.1084/jem.20020009
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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.
