Interleukin-13: Central Mediator of Allergic Asthma

American Association for the Advancement of Science (AAAS) - Tập 282 Số 5397 - Trang 2258-2261 - 1998
Marsha Wills‐Karp1, Jackie Luyimbazi1, Xueying Xu1, Brian Schofield1, Tamlyn Y. Neben1, Christopher L. Karp1, Debra D. Donaldson1
1M. Wills-Karp, J. Luyimbazi, X. Xu, B. Schofield, Department of Environmental Health Sciences, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD 21205, USA. T. Y. Neben and D. D. Donaldson, Immunology Department, Genetics Institute, Cambridge, MA 02140, USA. C. L. Karp, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA, and Department of Molecular Microbiology and Immunology, Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD 21205, USA.

Tóm tắt

The worldwide incidence, morbidity, and mortality of allergic asthma are increasing. The pathophysiological features of allergic asthma are thought to result from the aberrant expansion of CD4 + T cells producing the type 2 cytokines interleukin-4 (IL-4) and IL-5, although a necessary role for these cytokines in allergic asthma has not been demonstrable. The type 2 cytokine IL-13, which shares a receptor component and signaling pathways with IL-4, was found to be necessary and sufficient for the expression of allergic asthma. IL-13 induces the pathophysiological features of asthma in a manner that is independent of immunoglobulin E and eosinophils. Thus, IL-13 is critical to allergen-induced asthma but operates through mechanisms other than those that are classically implicated in allergic responses.

Từ khóa


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This work was supported by grants from NIH (HL58527) and the Center for Indoor Air Research to M.W.-K. We thank B. Annis and Z. Lu at Genetics Institute for murine rIL-13 and the Research Support Team at Genetics Institute for murine s13Rα2-Fc.