Cell‐surface bound pertussis toxin induces polyclonal T cell responses with high levels of interferon‐γ in the absence of interleukin‐12

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Abstract
Pertussis toxin (PTx), an exotoxin produced by Bordetella pertussis, has long been used as a mucosal adjuvant. We examined the T cell stimulatory properties of PTx in order to dissectits mechanisms of adjuvanticity. PTx or the B‐oligomer of PTx (PTxB) failed to activate purified murine CD4+ or CD8+ T cells, as measured by a lack of proliferation or expression of early T cell activation markers. However, these T cells proliferated extensively in response to the toxin in the presence of syngeneic DC, and proliferation was accompanied by a high level of IFN‐γ production in the absence of IL‐12. Interestingly, such responses were independent of signals mediated by MHC–TCR interaction. Both PTx and PTxB were found to bind stably to the surface of DC, and increased the adherence of DC to surrounding cells. These data suggest that polyclonal T cell responses mediated by the toxin are likely to be caused by the toxin bound on the surface of APC, either cross‐linking cell surface molecules on T cells, or directly stimulating T cells together with the co‐stimulatory molecules expressed on APC. B. pertussis may use this toxin as a mechanism to evade a specific immune response.

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