Summary of Section 5: Immunity  Cats resistant to FIP are known to have strong cell-mediated immunity (CMI), which can be measured by high levels of the cytokine interferon gamma (IFN-γ) in the serum. However, CMI is also likely to be involved in the pathogenesis of FIP, albeit at a tissue level, as evidenced by high IFN-γ concentration in FIP effusions. Single-nucleotide polymorphisms (SNPs) in the feline IFN-γ gene have been found to be associated with the outcome of FCoV infection, but these associations are not discriminatory enough to be beneficial to deduce susceptibility in individual cats, nor to guide breeding.  The role of humoral immunity in protecting against FIP is ambiguous. Maternally derived antibodies are thought to provide protection until kittens are about five to six weeks old, until they decline by six to eight weeks of age. Antibody development to FCoV takes 7 to 28 days post-infection. Following natural infection, antibody titres can decline to zero over a period of several months to years. In cats with pre-existing antibodies, ‘antibody-dependent enhancement’ (ADE) has been observed experimentally, resulting in a more rapid FIP progression and earlier death. However, in field studies, cats developed FIP on first exposure to FCoV (and thus did not have pre-existing antibodies), and some cats experienced repeated infections by FCoV and did not develop FIP, leading to the conclusion that ADE is likely to be an experimental phenomenon, but it still remains a concern for vaccine development.