We have also previously shown that colitogenic isolate 11168 infection followed by IFN-γ and/or IL-17 depletion leads to reciprocal upregulation of Campylobacter specific (but not autoreactive) Type2/IgG1 response.20 No treatment group developed significant C. jejuni specific IgG3 antibodies (Figure 1(c)). This evidence concerns the gene IL17A and infection.