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IL-13 Is a Susceptibility Factor forLeishmania majorInfection
Author(s) -
David J. Matthews,
Claire Emson,
Grahame J. McKenzie,
Helen E. Jolin,
Jenefer M. Blackwell,
Andrew N. J. McKenzie
Publication year - 2000
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.164.3.1458
Subject(s) - biology , immune system , leishmania major , immunology , inbred strain , transgene , interleukin 4 , genetically modified mouse , strain (injury) , leishmania , virology , gene , parasite hosting , genetics , anatomy , world wide web , computer science
Leishmania major infection is useful as an experimental model to define factors responsible for the development and maintenance of Th cell immune responses. Studies using inbred mouse strains have identified that the Th1 response characteristic of C57BL/6 mice results in healing, whereas BALB/c mice fail to control the infection due to the generation of an inappropriate Th2 response. We now demonstrate that IL-13 is a key factor in determining susceptibility to L. major infection. Overexpression of IL-13 in transgenic mice makes the normally resistant C57BL/6 mouse strain susceptible to L. major infection even in the absence of IL-4 expression. This susceptibility correlates with a suppression of IL-12 and IFN-gamma expression. Furthermore, using BALB/c mice deficient in the expression of IL-4, IL-13, or both IL-13 and IL-4, we demonstrate that IL-13-deficient mice are resistant to infection and that there is an additive effect of deleting both IL-4 and IL-13.

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