strigosum. The first 2 principal components accounted for 67% of total variation in the immune variables (proportion of variance ± SD: PC-1 = 0·44 ± 1·63 and PC-2 = 0·23 ± 1·164). The first component was equally explained by eosinophils (coeff. = −0·47), lymphocytes (−0·48), mucus IgA (−0·43) and IgG (−0·41), while the second component was driven by IFN-γ (−0·71) and PLX3397 IL-4 (−0·56). Unexpected was the positive association between IFN-γ and IL-4 (also supported by the significant correlation of their Ct values, Pearson’s r = 59%n = 28, P < 0·01). Graphidium strigosum abundance was negatively related to the first principal component (coeff. ± SE =

−0·238 ± 0·064, P < 0·01, Figure 7b), indicating a positive association with antibodies and peripheral leucocytes. No significant relationship was

observed with the second principal component. The analysis between helminth abundance and the immune variables selected in the PCA confirmed the positive correlation of the nematodes with IL-4, eosinophil and lymphocyte AZD2281 cell line (coeff. ± SE: −0·145 ± 0·061, 0·380 ± 0·118 and 0·321 ± 0·135, respectively, for all P < 0·05), once corrected for the random effect of the host code (ID). No significant relationship was observed with IFN-γ or antibodies. These general findings suggest that cytokines, leucocytes and antibodies modulate the dynamics of parasite infection; however, antibodies or leucocytes alone are not sufficient for parasite clearance. We used a controlled experimental approach to explore the dynamics of primary infections and the immune response of rabbits with the gastrointestinal nematodes T. retortaeformis CYTH4 and G. strigosum over a period of 120 days. Rabbits mounted a robust local and systemic immune response to T. retortaeformis that resulted in the almost complete clearance

of the nematode by the end of the trial. In contrast, G. strigosum persisted at high abundance throughout the infection, and this pattern was associated with relatively high serum but low mucus antibodies. Overall, the dynamics of infection of these nematodes were consistent with the age–intensity relationships we observed in our free-living rabbit population. Rabbits immuno-regulate the abundance of T. retortaeformis, and this results in the turnover of the age–intensity curve with a decrease in adult parasites in older rabbits (10). In contrast, immunity is not effective in removing G. strigosum, and intensities increased as a function of accumulated exposure to the parasite (11). The current study confirmed that the dynamics of infection in these two species can be explained by differences in the intensity and kinetics of the immune profile towards these parasites.