Interleukin-5 is necessary for eosinophilia induced by cyclophosphamide in immunized mice

Immunology. 1993 Jul;79(3):452-8.


Interleukin-5 (IL-5) has an important role in the induction of eosinophilia, which is associated with parasitic infestations and with allergic conditions, and which can be induced in a number of experimental systems. One of these model systems involves the administration of cyclophosphamide (CY) to immunized animals. In order to assess the role of IL-5 in this model, eosinophilia was induced in vivo and cell suspensions of spleens or lymph nodes were stimulated in vitro. IL-5 protein secretion was detected by bioassay using an IL-5-dependent cell line (T88-m), and mRNA was assessed by reverse transcription and polymerase chain reaction (RT-PCR). The production of IL-5 protein and mRNA were greatly enhanced in the cells from mice given CY with ovalbumin (OVA), compared with mice given either agent alone. IL-5 protein and mRNA were increased both in spleen and in lymph node cells, and in response either to OVA or to polyclonal stimuli. Further evidence for the importance of IL-5 in this model of eosinophilia was provided by experiments with monoclonal antibodies (mAb) in vivo. A single injection of an IL-5-specific mAb at the time of immunization completely abolished the eosinophilia. By contrast, a monoclonal antibody to IL-4 had no effect. These experiments indicate that IL-5 is required for the eosinophilia induced by CY in immunized mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / immunology
  • Base Sequence
  • Cells, Cultured
  • Cyclophosphamide
  • Eosinophilia / chemically induced
  • Eosinophilia / immunology*
  • Female
  • Interleukin-5 / biosynthesis
  • Interleukin-5 / genetics
  • Interleukin-5 / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Molecular Sequence Data
  • Polymerase Chain Reaction
  • RNA, Messenger / analysis


  • Antibodies, Monoclonal
  • Interleukin-5
  • RNA, Messenger
  • Cyclophosphamide