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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, Jahrgang 6, 17.06.2016, S. 28058.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Sellau, J, Alvarado, CF, Hoenow, S, Mackroth, MS, Kleinschmidt, D, Huber, S & Jacobs, T 2016, 'IL-22 dampens the T cell response in experimental malaria', SCI REP-UK, Jg. 6, S. 28058. https://doi.org/10.1038/srep28058

APA

Sellau, J., Alvarado, C. F., Hoenow, S., Mackroth, M. S., Kleinschmidt, D., Huber, S., & Jacobs, T. (2016). IL-22 dampens the T cell response in experimental malaria. SCI REP-UK, 6, 28058. https://doi.org/10.1038/srep28058

Vancouver

Sellau J, Alvarado CF, Hoenow S, Mackroth MS, Kleinschmidt D, Huber S et al. IL-22 dampens the T cell response in experimental malaria. SCI REP-UK. 2016 Jun 17;6:28058. https://doi.org/10.1038/srep28058

Bibtex

@article{cefb3c428879442a9a2ab010578643b7,
title = "IL-22 dampens the T cell response in experimental malaria",
abstract = "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.",
keywords = "Journal Article",
author = "Julie Sellau and Alvarado, {Catherine Fuentes} and Stefan Hoenow and Mackroth, {Maria Sophie} and D{\"o}rte Kleinschmidt and Samuel Huber and Thomas Jacobs",
year = "2016",
month = jun,
day = "17",
doi = "10.1038/srep28058",
language = "English",
volume = "6",
pages = "28058",
journal = "SCI REP-UK",
issn = "2045-2322",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

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 -