Porcine neonatal coccidiosis is caused by the protozoan Isospora suis and affects mainly piglets in the first three weeks of life. High morbidity with diarrhoea and reduced weight gain lead to economic losses, affecting pig-breeding worldwide. Infection causes damage of the mucosal surface in the jejunum and ileum and transient non-haemorrhagic diarrhoea. Secondary infections with other enteric pathogens may lead to increased mortality. Despite its economic and veterinary importance, the immunology of porcine isosporosis is still poorly understood. A striking feature of the infection is the rapidly increasing age resistance prohibiting the development of clinical disease in piglets older than 3-4 weeks irrespective of the immune status. It can be hypothesised that the development of the innate immune system in the first weeks of life and subsequently its interplay with the adaptive immune system is closely related to this phenomenon. Infections with I. suis induce migration of TcR-gammadelta(+) cells to the gut during primary infection and lead to induction of IFN-gamma production by TcR-gammadelta(+) cells and CD4(+) T-helper cells in blood and various lymphoid tissues. Like in other coccidial infections both innate as well as adaptive response mechanisms are activated during infection. They might be both not completely developed in the first weeks of life and therefore leaving a time frame for successful infection.