gms | German Medical Science

During a malaria infection the balance between pro-inflammatory and anti inflammatory factors is crucial, since the disruption of this balance leads to pathology. A key element of these immunoregulatory mechanisms is the IL 10 cytokine family, which includes IL-22. Even though the expression of IL-22 is restricted to cells of the hematopoietic system, a specific IL-22 receptor on immune cells has not yet been identified. The known receptor (IL 22R1) is expressed on non-hematopoietic cells and plays an essential role in regulating the homeostasis. Important to mention is the existence of a soluble IL-22 receptor 2 (IL 22R2), which counteracts the binding between IL-22 and IL 22R1.

In serum samples of P. falciparum infected individuals as well as in the serum of P. berghei ANKA (PbA) infected mice IL-22 levels were elevated. At least in the mouse model we identified splenic γδ Tcells to be the main producers of IL-22.

Depending on the bioavailability of IL-22, a change in the parasitemia of PbA or P. yoelii NL (PyNL) infected mice could have been identified. The parasitemia was reduced in the absence of IL 22. Whereas IL-22R2 ko mice, which have higher IL-22 level in the serum suffer from an increased parasitemia.

Despite of the lower parasitemia in IL-22 ko mice, the survival rate of these mice is decreased during a PbA infection, which was reflected by a higher incidence of cerebral symptoms.

In the absence of IL-22 the immune response to malaria infection in mice is altered. This was clearly evident by higher plasma levels of IL-10, IL-17, IL12/IL23p40 and by an increased activation of T cells in PbA infected IL-22 ko mice. Considering the altered T cell response in IL-22 ko mice, we postulate a link between IL 22 and the adaptive immune system, which is currently not identified.