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*
Department of Immunology, University of Glasgow, Western Infirmary, Glasgow, Scotland, United Kingdom;
Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104;
Department of Microbiology and Immunology, University of California, San Francisco, CA 94122;
§
Department of Immunology, University of Cape Town, Cape Town, South Africa; and
¶
Department of Immunology, Strathclyde Institute for Biomedical Sciences, University of Strathclyde, Glasgow, Scotland, United Kingdom
Previous studies demonstrate that aluminium hydroxide adjuvant
(alum) produces increased Th1 responses in IL-4-deficient mice compared
with wild-type animals, although the continued production of IL-5 by
spleen cells from these mice also indicates that Th2 responses are
induced. In the present study, we demonstrate that alum can induce
Th2-associated IL-4 and IL-5 production in the absence of IL-4
signaling in mice deficient in either IL-4R
or Stat6. The Th2
responses observed could not be due to IL-13 as IL-13 responses are
also impaired in IL-4R- and Stat6-deficient mice. We also detected
higher levels of IL-4 in IL-4R gene-deficient, though not
Stat6-deficient, mice compared with their wild-type counterparts. The
increased levels of IL-4 could be explained by the IL-4R being
unavailable to neutralize this cytokine in IL-4R-deficient mice.
While levels of IL-5 production in IL-4R- or Stat6-deficient mice
were similar to IL-4-deficient and wild-type mice, other type
2-associated responses, which are largely or wholly IL-4 dependent,
such as the production of IgG1 or IgE Abs, were either reduced or
absent. We conclude that alum adjuvants can induce IL-4 production and
Th2 responses independently of IL-4 or IL-13, negating the requirement
for an early source of IL-4 in the Th2 response induced by this
adjuvant.
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