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Background  Pertussis toxin (PTX), an exotoxin of  Bordetella pertussis , enhances the development of experimental autoimmune diseases such as experimental autoimmune uveitis (EAU) and experimental autoimmune encephalomyelitis (EAE) in rodent models. The mechanisms of the promotion of experimental autoimmune diseases by PTX may be based upon PTX-induced disruption of the blood eye/brain barriers facilitating the infiltration of inflammatory cells, the modulation of inflammatory cell migration and the enhancement of the activation of inflammatory cells. We hypothesized that the facilitation of experimental autoimmunity by PTX suggests that its influence on the  in vivo  immune response to auto-antigen may differ from its influence on non-self antigens.    Methodology/Principal Findings  We have evaluated the effect of PTX on the simultaneous generation of delayed type hypersensitivity (DTH) responses and autoimmune responses to uveitogenic interphotoreceptor retinoid binding protein peptide (IRBP 161–180 ), encephalitogenic myelin oligodendrocyte glycoprotein peptide (MOG 35–55 ) or ovalbumin (OVA). PTX injection of mice immunized to IRBP peptide 161–180  led to (i) the development of EAU as shown by histopathology of the retina, (ii) pro-inflammatory cytokine production by splenocytes in response to IRBP peptide  161–180 , and (iii) symptomatic EAE in mice immunized with encephalitogenic MOG peptide 35–55 . However, mice that received PTX had a reduced DTH response to IRBP 161–180  peptide or MOG peptide 35–55  when challenged distal to the site affected by autoreactive T cells. Moreover, footpad challenge with MOG 35–55  peptide reduced EAE in mice immunized with MOG peptide. In contrast, the use of PTX when immunizing with OVA protein or an OVA immunogenic peptide did not affect the DTH response to OVA.    Conclusions/Significance  The results suggest that that the reduced DTH response in mice receiving PTX may be specific for autoantigens and autoantigen-reactive T cells are diverted away from ectopic sites that received the autoantigen and towards the tissue site of the autoantigen.

Paradoxical Effect of Pertussis Toxin on the Delayed Hypersensitivity Response to Autoantigens in Mice