Generation and Analysis of Interleukin-4 Deficient Mice

TLDR

Interleukin‑4 drives hematopoietic cell growth and directs immunoglobulin class switching to IgG1 and IgE. Researchers created IL‑4 knockout mice to assess the cytokine’s in vivo role. The IL‑4‑deficient mice displayed normal T and B cell development but had markedly reduced serum IgG1 and IgE, lost IgG1 dominance in T‑cell‑dependent responses, and failed to produce IgE after nematode infection, indicating that only some in‑vitro IL‑4 functions are essential for immune physiology in vivo.

Abstract

Interleukin-4 (IL-4) promotes the growth and differentiation of many hematopoietic cells in vitro; in particular, it directs the immunoglobulin (Ig) class switch to IgG1 and IgE. Mice homozygous for a mutation that inactivates the IL-4 gene were generated to test the requirement for IL-4 in vivo. In the mutant mice T and B cell development was normal, but the serum levels of IgG1 and IgE were strongly reduced. The IgG1 dominance in a T cell-dependent immune response was lost, and IgE was not detectable upon nematode infection. Thus, some but not all of the in vitro properties of IL-4 are critical for the physiology of the immune system in vivo.