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IL‐15‐IgG2b fusion protein accelerates and enhances a Th2 but not a Th1 immune response in vivo, while IL‐2‐IgG2b fusion protein inhibits both

We have explored how IL‐15 influences Th1 or Th2 type immune response in vivo. Intraperitoneal application of an IL‐15‐IgG2b fusion protein (FP) to mice did neither significantly affect the footpad swelling nor the production of hemagglutinizing antibodies in a delayed type hypersensitivity reaction to sheep red blood cells. In contrast, in an established murine Th2 model of sensitization to ovalbumin (OVA), IL‐15‐IgG2b FP plus OVA sensitization resulted in massively accelerated and enhanced allergen‐specific IgE and IgG1 antibody production. In vitro, stimulation of spleen cells from OVA‐sensitized mice with OVA+IL‐15 or OVA+IL‐15‐IgG2b resulted in a significantly enhanced IgE production. IL‐4 secretion was significantly induced by IL‐15 but not by IL‐15‐IgG2b. An IL‐2‐IgG2b FP with the same Fc tail as the IL‐15‐IgG2b FP was used as control in both models. In striking contrast to the IL‐15‐IgG2b FP, IL‐2‐IgG2b significantly inhibited the Th2 type antibody production in vivo. The current study suggests that IL‐15‐IgG2b may be employed as a potent accelerator and enhancer of Th2 type immune responses in vivo, while IL‐2‐IgG2b can suppress the latter.