gms | German Medical Science

12th Malaria Meeting

Malaria Group / Section Antiparasitic Chemotherapy of the Paul-Ehrlich-Society (PEG e. V.) in cooperation with the German Society for Tropical Medicine and International Health (DTG e. V.) and the German Society for Parasitology (DGP e. V.)

14.11. - 15.11.2014, Bonn

IL-22 modifies the course of experimental malaria

Meeting Abstract

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  • Julie Sellau - Bernhard-Nocht-Institute for Tropical Medicine, Hamburg, Germany
  • Samuel Huber - University Medical Center Hamburg-Eppendorf, I. Department of Medicine, Hamburg, Germany
  • Thomas Jacobs - Bernhard-Nocht-Institute for Tropical Medicine, Hamburg, Germany

12th Malaria Meeting. Bonn, 14.-15.11.2014. Düsseldorf: German Medical Science GMS Publishing House; 2014. Doc14mal20

doi: 10.3205/14mal20, urn:nbn:de:0183-14mal208

Published: December 17, 2014

© 2014 Sellau et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



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.