IL-22 dampens the T cell response in experimental malaria.
A tight regulation between the pro- and anti-inflammatory immune responses during plasmodial infection is of crucial importance, since a disruption leads to severe malaria pathology. IL-22 is a member of the IL-10 cytokine family, which is known to be highly important in immune regulation. We could detect high plasma levels of IL-22 in Plasmodium falciparum malaria as well as in Plasmodium berghei ANKA (PbA)-infected C57BL/6J mice. The deficiency of IL-22 in mice during PbA infection led to an earlier occurrence of cerebral malaria but is associated with a lower parasitemia compared to wt mice. Furthermore, at an early time point of infection T cells from PbA-infected Il22(-/-) mice showed an enhanced IFNγ but a diminished IL-17 production. Moreover, dendritic cells from Il22(-/-) mice expressed a higher amount of the costimulatory ligand CD86 upon infection. This finding can be corroborated in vitro since bone marrow-derived dendritic cells from Il22(-/-) mice are better inducers of an antigen-specific IFNγ response by CD8(+) T cells. Even though there is no IL-22 receptor complex known on hematopoietic cells, our data suggest a link between IL-22 and the adaptive immune system which is currently not identified.
Bernhard-Nocht-Institute for Tropical Medicine, Bernhard-Nocht-Straße 74, 20359 Hamburg, Germany.
Julie
J
Sellau
Bernhard-Nocht-Institute for Tropical Medicine, Bernhard-Nocht-Straße 74, 20359 Hamburg, Germany.
Catherine Fuentes
CF
Alvarado
Bernhard-Nocht-Institute for Tropical Medicine, Bernhard-Nocht-Straße 74, 20359 Hamburg, Germany.
Stefan
S
Hoenow
Bernhard-Nocht-Institute for Tropical Medicine, Bernhard-Nocht-Straße 74, 20359 Hamburg, Germany.|University Medical Center Hamburg-Eppendorf, I. Department of Medicine, Martinistraße 52, 20246 Hamburg, Germany.
Maria Sophie
MS
Mackroth
University Medical Center Hamburg-Eppendorf, I. Department of Medicine, Martinistraße 52, 20246 Hamburg, Germany.
Dörte
D
Kleinschmidt
University Medical Center Hamburg-Eppendorf, I. Department of Medicine, Martinistraße 52, 20246 Hamburg, Germany.
Samuel
S
Huber
Bernhard-Nocht-Institute for Tropical Medicine, Bernhard-Nocht-Straße 74, 20359 Hamburg, Germany.
Thomas
T
Jacobs
D000818:Animals; D051940:B7-2 Antigen / Q000378:metabolism; D001854:Bone Marrow Cells / Q000166:cytology; D018414:CD8-Positive T-Lymphocytes / Q000166:cytology / Q000187:drug effects / Q000276:immunology*; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D004912:Erythrocytes / Q000166:cytology / Q000378:metabolism; D007371:Interferon-gamma / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D007378:Interleukins / Q000097:blood / Q000172:deficiency / Q000235:genetics*; D008070:Lipopolysaccharides / Q000633:toxicity; D008288:Malaria / Q000276:immunology / Q000401:mortality / Q000473:pathology* / Q000662:veterinary; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018512:Parasitemia / Q000469:parasitology / Q000473:pathology; D010962:Plasmodium berghei / Q000276:immunology / Q000502:physiology*; D016053:RNA, Protozoan / Q000302:isolation & purification / Q000378:metabolism; D013154:Spleen / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D015996:Survival Rate; D000097043:Interleukin-22
D051940:B7-2 Antigen; D007371:Interferon-gamma; D020381:Interleukin-17; D007378:Interleukins; D008070:Lipopolysaccharides; D016053:RNA, Protozoan; D000097043:Interleukin-22