Il12a KO Mice

Catalog Number: C001213

Strain Name: C57BL/6NCya-Il12aem1/Cya

Genetic Background: C57BL/6NCya

Reproduction: Homozygote x Homozygote

 

Strain Description

The interleukin 12A (IL12A or IL12p35) gene encodes the subunits of cytokines IL-12 and IL-35, which act on T cells and natural killer (NK) cells and have extensive biological activity. IL-12 is a heterodimer composed of the p35 subunit encoded by the IL12A gene and the p40 subunit, a member of the cytokine receptor family encoded by the IL12B gene. It is essential for non-T cell-dependent interferon-gamma (IFN-γ) induction and is also crucial for the differentiation of helper T cells (Th1 and Th2). On the other hand, the primary function of IL-35 is to suppress the inflammatory response of immune cells. IL12A also affects cardiovascular diseases by regulating inflammation, including heart fibrosis and myocardial infarction. Mutations in the IL12A gene are associated with susceptibility to certain infectious and autoimmune diseases [1].

This model is an Il12a gene knockout mouse, created using gene-editing technology to knock out the homologous Il12a gene of the human IL12A gene in mice. According to the literature, the deletion of Il12a in this mouse model leads to the loss of the biological effects of IL-12 and IL-35, reduced NK cell responses, altered differentiation of effector T cells, and increased susceptibility to parasitic infections. Additionally, this model cannot exhibit delayed-type hypersensitivity (DTH) reactions induced by the interaction of effector T cells with antigens [2]. The homozygous mice are viable and fertile.

Strain Strategy

The Il12a gene is located on chromosome 3 in mice. Using gene-editing technology, exons 3 ~ 7 of this gene were knocked out.


Application

  • Cardiovascular Disease Research;
  • Autoimmune Disease Research;
  • Infectious Disease Research;
  • Immune Cells and Systems Research.

 

References
[1]Ohman H, Bailey R, Natividad A, Ragoussis J, Johnson LL, Tiitinen A, Halttunen M, Paavonen J, Surcel HM. Effect of IL12A and IL12B polymorphisms on the risk of Chlamydia trachomatis-induced tubal factor infertility and disease severity. Hum Reprod. 2012 Jul;27(7):2217-23.
[2]Mattner F, Magram J, Ferrante J, Launois P, Di Padova K, Behin R, Gately MK, Louis JA, Alber G. Genetically resistant mice lacking interleukin-12 are susceptible to infection with Leishmania major and mount a polarized Th2 cell response. Eur J Immunol. 1996 Jul;26(7):1553-9.