II4ra Knockout

Constitutive Knockout

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The NIAID Exchange Program has closed and live production of this model has ceased. This webpage is retained for historical reference, but this model is not available from Taconic.

Model #
Genotype
Nomenclature

4177-F

ko/ko

BALB/cJ-Il4ra^tm1Sz
4177-M

ko/ko

BALB/cJ-Il4ra^tm1Sz

Model Description

The alpha chain of the interleukin 4 receptor (IL-4Ra) is a subunit shared by both IL-4 and IL-13 receptors, which accounts for many of their overlapping biological functions. Thus, in contrast to an IL-4 knockout mouse, the IL-4Ra knockout blocks the function of both cytokines. Parallel studies comparing the immune responses of BALB/c IL-4 and IL-4Ra mice have revealed a unique role for IL-13 in allergic responses, and susceptibility to infection with Nippostrongylus brasiliensis, Schistosoma mansoni, and to some strains of Leishmania major parasites. While T helper 2 (Th2) are markedly diminished in IL-4Ra-/- mice, IL-4 production can readily be detected. There appears to be an IL-4-independent induction of IL-4 pathway taking place in NK T cells and also in conventional, naive CD4+ T cells.

Origin:

The BALB/cJ IL-4 Ra KO mouse was generated by Nancy Noben-Trauth at Jackson Laboratory in 1997 and analyzed in the Laboratory of Immunology, NIAID, NIH with Hua Gua and William Paul. The targeting vector, which deleted exons 6-9 of the gene, was transfected into BALB/c-I ES cells (derived by Birgit Ledermann at Novartis Pharmaceuticals). The chimeric founders were crossed to BALB/cJ mice and then intercrossed to generate offspring homozygous for the targeted allele. The IL-4Ra-/- mice are therefore a genetically pure BALB/cJ strain. The line was derived by embryo transfer into the NIAID barrier facility at Taconic in 2000.

Availability:

This model is no longer available.

Color:

Albino or White

Species:

Mouse

Initial Publication:

Noben-Trauth N, et al.: An interleukin 4 (IL-4)-independent pathway for CD4+ T cell IL-4 production is revealed in IL-4 receptor-deficient mice; Proc. Natl. Acad. Sci, USA, 1997:94(9):10838-43.

Noben-Trauth N, Paul WE, and Sacks DL: IL-4- and IL-4 receptor-deficient BALB/c mice reveal differences in susceptibility to Leishmania major parasite substrains; J. Immunolo. 1999:162(10):6132-40.

Noben-Trauth, N., J.Hu-Li, and W. E. Paul. 2000. Conventional, naïve CD4+ T cells provide an initial source of IL-4 during Th2 differentiation; J. Immunolo. 165:3620-3625.