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*
Department of Biochemistry, Imperial College of Science, Technology and Medicine, South Kensington, London, United Kingdom;
The Chiron Vaccines Immunological Research Institute, Via Fiorentina, Siena, Italy; and
Department of Medical Microbiology and Immunology, University of Goteborg, Goteborg, Sweden
The ability of enterotoxin-based mucosal adjuvants to induce
CD8+ MHC class I-restricted CTL responses to a codelivered
bystander Ag was examined. Escherichia coli heat-labile
toxin (LT), or derivatives of LT carrying mutations in the A subunit
(LTR72, LTK63), were tested in parallel with cholera toxin (CT) or a
fusion protein consisting of the A1 subunit of CT fused to the Ig
binding domain of Staphylococcus aureus protein A
(called CTA1-DD). Intranasal (i.n.) immunization of C57BL/6 mice with
CT, CTA1-DD, LT, LTR72, LTK63, but not rLT-B, elicited MHC class
I-restricted CD8+ T cell responses to coadministered OVA or
the OVA CTL peptide SIINFEKL (OVA257–264). CT, LT, and
LTR72 also induced CTL responses to OVA after s.c. or oral
coimmunization whereas LTK63 only activated responses after s.c.
coimmunization. rLT-B was unable to adjuvant CTL responses to OVA or
OVA257–264 administered by any route. Mice treated with an
anti-CD4 mAb to deplete CD4+ T cells mounted
significant OVA-specific CTL responses after i.n. coadministration of
LT with OVA or OVA257–264. Both 51Cr release
assays and IFN-
enzyme-linked immunospot assays indicated that
IFN--/- and IL-12 p40-/- gene knockout
mice developed CTL responses equivalent to those detected in normal
C57BL/6 mice. The results highlight the versatility of toxin-based
adjuvants and suggest that LT potentiates CTL responses independently
of IL-12 and IFN- and probably by a mechanism unrelated to
cross-priming.
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