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Blood, Vol. 95 No. 5 (March 1), 2000:
pp. 1600-1607
Interleukin 5 regulates the isoform expression of its own receptor
 -subunit
Jan Tavernier,
José Van der Heyden,
Annick Verhee,
Guy Brusselle,
Xaveer Van Ostade,
Joël Vandekerckhove,
Janet North,
Sara
M. Rankin,
A. Barry Kay, and
Douglas S. Robinson
From the Flanders Interuniversity Institute for Biotechnology and
Department of Respiratory Diseases, University of Ghent, Belgium;
Allergy and Clinical Immunology, National Heart and Lung Institute and
Leukocyte Biology, BioMedical Sciences Division, Imperial College
School of Medicine, London, UK.
The receptor for interleukin 5 (IL-5) consists of a
cytokine-specific  chain (IL-5R) and a signaling  chain, which
is shared with interleukin 3 (IL-3) and granulocyte-macrophage
colony-stimulating factor (GM-CSF). These 3 cytokines can act in
eosinophil development and activation in vitro, but gene deletion or
antibody blocking of IL-5 largely ablates eosinophilic responses in
models of allergic disease or helminth infection. We investigated
factors acting in differential IL-5R gene splicing to generate
either the membrane-anchored isoform (TM-IL-5R) which
associates with the common chain to allow IL-5 responsiveness, or
a secreted, antagonist variant (SOL-IL-5R). In a murine myeloid cell
line (FDC-P1), transfected with minigenes allowing expression of either
IL-5R variant, IL-5 itself, but not IL-3 or GM-CSF, stimulated a
reversible switch toward expression of TM-IL-5R. A switch from
predominantly soluble isoform to TM-IL-5R messenger RNA (mRNA)
expression was also seen during IL-5-driven eosinophil development from
human umbilical cord blood-derived CD34+ cells; this was
accompanied by surface expression of IL-5R and acquisition of
functional responses to IL-5. IL-3 and GM-CSF also supported eosinophil
development and up-regulation of TM-IL-5R mRNA in this system, but
this was preceded by expression of IL-5 mRNA and was inhibited by
monoclonal antibody to IL-5. These data suggest IL-5-specific
signaling, not shared by IL-3 and GM-CSF, leading to a switch toward
up-regulation of functional IL-5R and, furthermore, that IL-3 and
GM-CSF-driven eosinophil development is dependent on IL-5, providing an
explanation for the selective requirement of IL-5 for expansion of the
eosinophil lineage.
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