IL-22 dampens the T cell response in experimental malaria
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IL-22 dampens the T cell response in experimental malaria. / Sellau, Julie; Alvarado, Catherine Fuentes; Hoenow, Stefan; Mackroth, Maria Sophie; Kleinschmidt, Dörte; Huber, Samuel; Jacobs, Thomas.
In: SCI REP-UK, Vol. 6, 17.06.2016, p. 28058.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - IL-22 dampens the T cell response in experimental malaria
AU - Sellau, Julie
AU - Alvarado, Catherine Fuentes
AU - Hoenow, Stefan
AU - Mackroth, Maria Sophie
AU - Kleinschmidt, Dörte
AU - Huber, Samuel
AU - Jacobs, Thomas
PY - 2016/6/17
Y1 - 2016/6/17
N2 - 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.
AB - 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.
KW - Journal Article
U2 - 10.1038/srep28058
DO - 10.1038/srep28058
M3 - SCORING: Journal article
C2 - 27311945
VL - 6
SP - 28058
JO - SCI REP-UK
JF - SCI REP-UK
SN - 2045-2322
ER -