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* Departments of Microbiology and Oral Biology, Immunobiology Vaccine Center, University of Alabama, Birmingham, AL 35294;
Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan;
Division of Mucosal Immunology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, Tokyo, Japan;
Department of Oral Medicine, Nihon University School of Dentistry at Matsudo, Chiba, Japan; and
¶ Department of Microbiology, Jissen Women’s College, Tokyo, Japan
Native cholera toxin (nCT) and the heat-labile toxin 1 (nLT) of
enterotoxigenic Escherichia coli are
AB5-type enterotoxins. Both nCT and nLT are effective
adjuvants that promote mucosal and systemic immunity to protein Ags
given by either oral or nasal routes. Previous studies have shown that
nCT as mucosal adjuvant requires IL-4 and induces CD4-positive
(CD4+) Th2-type responses, while nLT up-regulates Th1 cell
production of IFN-
and IL-4-independent Th2-type responses. To
address the relative importance of the A or B subunits in
CD4+ Th cell subset responses, chimeras of CT-A/LT-B and
LT-A/CT-B were constructed. Mice nasally immunized with CT-A/LT-B or
LT-A/CT-B and the weak immunogen OVA developed OVA-specific, plasma IgG
Abs titers similar to those induced by either nCT or nLT. Both
CT-A/LT-B and LT-A/CT-B promoted secretory IgA anti-OVA Ab, which
established their retention of mucosal adjuvant activity. The CT-A/LT-B
chimera, like nLT, induced OVA-specific mucosal and peripheral
CD4+ T cells secreting IFN- and IL-4-independent
Th2-type responses, with plasma IgG2a anti-OVA Abs. Further,
LT-A/CT-B, like nCT, promoted plasma IgG1 more than IgG2a and IgE Abs
with OVA-specific CD4+ Th2 cells secreting high levels of
IL-4, but not IFN-. The LT-A/CT-B chimera and nCT, but not the
CT-A/LT-B chimera or nLT, suppressed IL-12R expression and IFN-
production by activated T cells. Our results show that the B subunits
of enterotoxin adjuvants regulate IL-12R expression and subsequent Th
cell subset responses.
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