Therefore, the lack of involvement of PMNs in the protective response to cytokine treatment which we found at day 7 after primary C. albicans infection of the Tg mice may more closely mimic the reality of the host-pathogen interaction found in HIV-infected patients with established OPC, and provides evidence to support the concept that the mobilization of PMNs may not be the primary underlying mechanism by which IL-17 mediates antifungal effects at this stage of infection [35]. Here, IL17A is linked to infection.