Mice homozygous for this Ebi3-mutant allele are viable and fertile with the donating investigator reporting no overt autoimmunity or inflammatory disease associated with the mutation. No RNA from the targeted gene is observed in splenocytes isolated from homozygotes. Ebi3-deficiency leads to impaired Treg activity with failure to control homeostatic proliferation. Homozygotes exhibit decreased numbers and function of invariant natural killer T cells (iNKT); stimulated iNKT cells show impaired IL-4 production both in vivo and in vitro. Homozygotes are resistant to oxazolone-induced colitis (mediated primarily by T helper (Th) 2-type cytokine production by iNKT cells), whereas Ebi3-deficiency shows no affect on trinitrobenzene sulfonic acid-induced colitis (a predominantly Th1-mediated colitis model). These Ebi3-mutant strains may be useful in studying Treg function, IL12 heterodimeric cytokines (such as IL-35 and IL-27),IFNgamma production, and Th1/Th2 immune responses (including inflammatory bowel disease).
Of note, Ebi3-mutant mice are also be available on a BALB/c congenic background (see Stock No. 008701).
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
