Fcgr2b (FcγRII) - Model 580

Constitutive Knock Out

Fcgr2b (FcγRII) 580 Constitutive Knock Out Mouse Model

C57BL/6 Background

  • Model #
  • Genotype
  • Nomenclature
  • 580-F
    ko/ko
    B6.129S4-Fcgr2btm1TtK N12
  • 580-M
    ko/ko
    B6.129S4-Fcgr2btm1TtK N12
  • The mice are deficient in FcgRIIß protein which is a low affinity immunoglobulin G receptor
  • The FcgRIIß protein inhibits the activation of disparate effector functions such as phagocytosis, antibody dependent cytotoxicity and release of inflammatory mediators and it is known to function as an inhibitory receptor on B cells and mast cells
  • This inhibitory pathway for activation of several immune effector responses is dysfunctional, resulting in the inability to regulate antibody levels in response to antigenic stimuli dependent on IgG immune complexes
  • Useful for studying the feedback inhibition pathways that regulate antibody production and in studies of allergic and autoimmune disorders
  • The mice are fertile and develop normally
  • These mice carry the H2b haplotype
Orders by weight: Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.

Origin:

The Fcgr2b mouse was developed in the laboratory of T. Takai of Okayama University in 1995. The model was created by targeting the Fcgr2b gene in J1 ES cells. Taconic received pregnant females from Okayama University in November 1996 for use by the laboratory of J.V. Ravetch. Heterozygotes on a hybrid 129 x C57BL/6 background were intercrossed to generate homozygous targeted mutation mice. The mice were then backcrossed twelve generations (N12) to C57BL/6. The mice were derived by embryo transfer and are maintained by incrossing homozygous mice.

Genetics:

Wildtype for Nnt mutation

Color:

Black

Species:

Mouse

Initial Publication:

Takai, T, Ono, M, Hikida, M, Ohmori, H, Ravetch, J. (1996) Augmented humoral and anaphylactic responses in FcgRII-deficient mice. Nature, 379: 346-349.



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