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Enhanced Interleukin (IL)-13 Responses in Mice Lacking IL-13 Receptor α 2

Interleukin (IL)-13 has recently been shown to play important and unique roles in asthma, parasite immunity, and tumor recurrence. At least two distinct receptor components, IL-4 receptor (R)α and IL-13Rα1, mediate the diverse actions of IL-13. We have recently described an additional high affinity...

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Autores principales: Wood, Nancy, Whitters, Matthew J., Jacobson, Bruce A., Witek, JoAnn, Sypek, Joseph P., Kasaian, Marion, Eppihimer, Michael J., Unger, Michelle, Tanaka, Takashi, Goldman, Samuel J., Collins, Mary, Donaldson, Debra D., Grusby, Michael J.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2003
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193851/
https://www.ncbi.nlm.nih.gov/pubmed/12642602
http://dx.doi.org/10.1084/jem.20020906
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author Wood, Nancy
Whitters, Matthew J.
Jacobson, Bruce A.
Witek, JoAnn
Sypek, Joseph P.
Kasaian, Marion
Eppihimer, Michael J.
Unger, Michelle
Tanaka, Takashi
Goldman, Samuel J.
Collins, Mary
Donaldson, Debra D.
Grusby, Michael J.
author_facet Wood, Nancy
Whitters, Matthew J.
Jacobson, Bruce A.
Witek, JoAnn
Sypek, Joseph P.
Kasaian, Marion
Eppihimer, Michael J.
Unger, Michelle
Tanaka, Takashi
Goldman, Samuel J.
Collins, Mary
Donaldson, Debra D.
Grusby, Michael J.
author_sort Wood, Nancy
collection PubMed
description Interleukin (IL)-13 has recently been shown to play important and unique roles in asthma, parasite immunity, and tumor recurrence. At least two distinct receptor components, IL-4 receptor (R)α and IL-13Rα1, mediate the diverse actions of IL-13. We have recently described an additional high affinity receptor for IL-13, IL-13Rα2, whose function in IL-13 signaling is unknown. To better appreciate the functional importance of IL-13Rα2, mice deficient in IL-13Rα2 were generated by gene targeting. Serum immunoglobulin E levels were increased in IL-13Rα2(−/−) mice despite the fact that serum IL-13 was absent and immune interferon γ production increased compared with wild-type mice. IL-13Rα2–deficient mice display increased bone marrow macrophage progenitor frequency and decreased tissue macrophage nitric oxide and IL-12 production in response to lipopolysaccharide. These results are consistent with a phenotype of enhanced IL-13 responsiveness and demonstrate a role for endogenous IL-13 and IL-13Rα2 in regulating immune responses in wild-type mice.
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spelling pubmed-21938512008-04-11 Enhanced Interleukin (IL)-13 Responses in Mice Lacking IL-13 Receptor α 2 Wood, Nancy Whitters, Matthew J. Jacobson, Bruce A. Witek, JoAnn Sypek, Joseph P. Kasaian, Marion Eppihimer, Michael J. Unger, Michelle Tanaka, Takashi Goldman, Samuel J. Collins, Mary Donaldson, Debra D. Grusby, Michael J. J Exp Med Article Interleukin (IL)-13 has recently been shown to play important and unique roles in asthma, parasite immunity, and tumor recurrence. At least two distinct receptor components, IL-4 receptor (R)α and IL-13Rα1, mediate the diverse actions of IL-13. We have recently described an additional high affinity receptor for IL-13, IL-13Rα2, whose function in IL-13 signaling is unknown. To better appreciate the functional importance of IL-13Rα2, mice deficient in IL-13Rα2 were generated by gene targeting. Serum immunoglobulin E levels were increased in IL-13Rα2(−/−) mice despite the fact that serum IL-13 was absent and immune interferon γ production increased compared with wild-type mice. IL-13Rα2–deficient mice display increased bone marrow macrophage progenitor frequency and decreased tissue macrophage nitric oxide and IL-12 production in response to lipopolysaccharide. These results are consistent with a phenotype of enhanced IL-13 responsiveness and demonstrate a role for endogenous IL-13 and IL-13Rα2 in regulating immune responses in wild-type mice. The Rockefeller University Press 2003-03-17 /pmc/articles/PMC2193851/ /pubmed/12642602 http://dx.doi.org/10.1084/jem.20020906 Text en Copyright © 2003, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Wood, Nancy
Whitters, Matthew J.
Jacobson, Bruce A.
Witek, JoAnn
Sypek, Joseph P.
Kasaian, Marion
Eppihimer, Michael J.
Unger, Michelle
Tanaka, Takashi
Goldman, Samuel J.
Collins, Mary
Donaldson, Debra D.
Grusby, Michael J.
Enhanced Interleukin (IL)-13 Responses in Mice Lacking IL-13 Receptor α 2
title Enhanced Interleukin (IL)-13 Responses in Mice Lacking IL-13 Receptor α 2
title_full Enhanced Interleukin (IL)-13 Responses in Mice Lacking IL-13 Receptor α 2
title_fullStr Enhanced Interleukin (IL)-13 Responses in Mice Lacking IL-13 Receptor α 2
title_full_unstemmed Enhanced Interleukin (IL)-13 Responses in Mice Lacking IL-13 Receptor α 2
title_short Enhanced Interleukin (IL)-13 Responses in Mice Lacking IL-13 Receptor α 2
title_sort enhanced interleukin (il)-13 responses in mice lacking il-13 receptor α 2
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193851/
https://www.ncbi.nlm.nih.gov/pubmed/12642602
http://dx.doi.org/10.1084/jem.20020906
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