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Division of Pulmonary Medicine, Allergy, and Clinical Immunology, Department of Pediatrics, Children’s Hospital Medical Center, Cincinnati, OH 45229
IL-13 is a Th2-derived pleiotropic cytokine that recently was shown
to be a key mediator of allergic asthma. IL-13 mediates its effects via
a complex receptor system, which includes the IL-4R 
-chain,
IL-4R, and at least two other cell surface proteins, IL-13R1 and
IL-13R2, which specifically bind IL-13. IL-13 has been reported to
have very limited effects on mouse B cells. It was unclear whether this
was due to a lack of receptor expression, a disproportionate relative
expression of the receptor components, or an additional subunit
requirement in B cells. To determine the requirements for IL-13
signaling in murine B cells, we examined IL-13-dependent Stat6
activation and CD23 induction in the murine B cell line, A201.1. A201.1
cells responded to murine IL-4 via the type I IL-4R, but were
unresponsive to IL-13, and did not express IL-13 receptor.
B220+ splenocytes also failed to signal in response to
IL-13 and did not express IL-13 receptor. We transfected A201.1 cells
with human IL-4R, IL-13R1, or both. Transfectants expressing
either human IL-4R or human IL-13R1 alone were unable to respond
or signal to IL-13. Thus, human IL-13R1 could not combine with the
endogenous murine IL-4R to generate a functional IL-13R. However,
cells transfected with both human IL-4R and IL-13R1 responded to
IL-13. Thus, the relative lack of IL-13 responsiveness in murine B
cells is due to a lack of receptor expression. Furthermore, the
heterodimeric interaction between IL-4R and IL-13R1 is species
specific.
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