IL21R is a type I cytokine receptor for IL21. Type 1 cytokines are involved in T cell proliferation, differentiation, and maintenance of memory population. Ligand binding of IL21R activates downstream signaling through the JAK/STAT pathway.

In this strain, developed by Drs. Manfred Kopf and Martin Hodge, a neomycin cassette replaces exons 2-5 of the targeted allele, Il21rtm1Kopf. Mice homozygous for the mutation are viable, fertile, and do not display any gross physical or behavioral abnormalities. 

OVA airway challenge and infection with gastrointestinal nematodes of Il21r-/- mice resulted in impaired Th2 type effector responses (i.e. reduced numbers of IL-4 producing cells, basophils, eosinophils, and intestinal granuloma). In contrast, no differences were observed in development of Th17 cells and organ-related autoimmunity in models of experimental allergic encephalitis (EAE) and myocarditis (EAM). Further studies showed that Il21r-/- mice were highly susceptible to chronic viral infection due to a defect in maintenance of polyfunctional anti-viral CD8 T cell responses. 
This strain may be useful for studying the role of IL21 in T and B cell responses to various pathogens and in models of allergies and autoimmunity.







When referencing the use of this strain, please be sure to use this citation: Frohlich A. et al., Blood 2007 109(5):2023-31.

OVA or parasite challenge of these Il21r knockout mice developed by Dr. Manfred Kopf results in impaired Th2 type effector responses. This strain may be useful for studying IL21 in T and B cell response to various pathogens and in models of allergies and autoimmunity.

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